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“PRELIMINARY PHYTOCHEMICAL INVESTIGATION & SHOTHAHARA (ANTI-INFLAMMATORY) EFFECT OF DEVADARU (CEDRUS DEODARA) ON ALBINO RATS AN EXPERIMENTAL STUDY ”. BY Dr. Shivaleela M.Kudari Dissertation submitted to the Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore. In partial fulfillment of Regulations for award of degree of AYURVEDA VACHASPATI M.D. IN DRAVYAGUNA Under the guidance of DR. KUBER. SANKH. M.D. (AYU) DEPARTMENT OF DRAVYA GUNA POST GRADUATE STUDIES & RESEARCH CENTER SHRI D.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE, GADAG-582103 2007

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“PRELIMINARY PHYTOCHEMICAL INVESTIGATION & SHOTHAHARA (ANTI-INFLAMMATORY) EFFECT OF DEVADARU (CEDRUS DEODARA) ON ALBINO RATS AN EXPERIMENTAL STUDY ” - Dr. Shivaleela M.Kudari, Department of Dravya Guna, Post Graduate Studies & Research Centre, D.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE,GADAG

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“PRELIMINARY PHYTOCHEMICAL INVESTIGATION

& SHOTHAHARA (ANTI-INFLAMMATORY) EFFECT

OF DEVADARU (CEDRUS DEODARA) ON ALBINO

RATS AN EXPERIMENTAL STUDY ”. BY

DDrr.. SShhiivvaalleeeellaa MM..KKuuddaarrii

Dissertation submitted to the Rajiv Gandhi University

of Health Sciences, Karnataka, Bangalore.

In partial fulfillment of Regulations for award of degree of

AAYYUURRVVEEDDAA VVAACCHHAASSPPAATTII MM..DD..

IN

DRAVYAGUNA

Under the guidance of

DR. KUBER. SANKH. M.D. (AYU)

DEPARTMENT OF DRAVYA GUNA

POST GRADUATE STUDIES & RESEARCH CENTER

SHRI D.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE, GADAG-582103

2007

Ayurmitra
TAyComprehended
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DECLARATION BY THE CANDIDATE

I hereby declare that this dissertation / thesis entitled “Preliminary Phitochemical

investigation & Shothara (anti-inflammatory) effect of devadaru

(cedrusdeodara) on Albino rats – an Experimental study is a bonafide and genuine

research work carried out by me under the guidance of Dr. Kuber Sankh. MD (Ayu),

Asst. Professor, Department of Dravyaguna, Shri D.G.M.A.M.C, PGS & RC, Gadag.

Date: Signature of the Candidate

PLACE: (DDrr.. SShhiivvaalleeeellaa MM..KKuuddaarrii))

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D.G.M.AYURVEDIC MEDICAL COLLEGE

POST GRADUATE STUDIES AND RESEARCH CENTRE

GADAG, 582 103

This is to certify that the dissertation entitled “Preliminary Phitochemical

investigation & Shothara (anti-inflammatory) effect of devadaru

(cedrusdeodara) on Albino rats – an Experimental study is a bonafide research

work done by Shivaleela. M. Kudari in partial fulfillment of the requirement for the

post graduation degree of “Ayurveda Vachaspati M.D. (Dravya Guna)” Under

Rajiv Gandhi University of Health Sciences, Bangalore, Karnataka.

Guide Dr. KUBER SANKH

M.D. (Ayu) Asst. Professor

Dept of Dravya Guna

DGMAMC, PGS&RC, GADAG

Date:

Place: Gadag

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J.S.V.V. SAMSTHE’S

D.G.M.AYURVEDIC MEDICAL COLLEGE

POST GRADUATE STUDIES AND RESEARCH CENTRE

GADAG, 582 103

Endorsement by the H.O.D,Principal/head of the

Institution

This is to certify that the dissertation entitled “Preliminary Phitochemical

investigation & Shothara (anti-inflammatory) effect of devadaru

(cedrusdeodara) on Albino rats - an Experimental study is a bonafide research

work done by Dr. Shivaleela M. Kudari under the guidance of

Dr. KUBER SANKH MD (Ayu), Asst. Professor, Department of Dravyaguna, in partial

fulfillment of the requirement for the post graduation degree of “Ayurveda

Vachaspati M.D. (Dravya Guna)” Under Rajiv Gandhi University of Health

Sciences, Bangalore, Karnataka.

(Dr. G.V. MULAGUND) (Dr. G.B. PATIL) Professor & H.O.D. Principal Dept of Dravya Guna DGM Ayurvedic Medical College, DGMAMC, PGS&RC. Gadag

Date: Date: Place: Gadag Place: Gadag

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© Copy right

Declaration by the Candidate

I here by declare that the Rajiv Gandhi University of Health Sciences,

Karnataka shall have the rights to preserve, use and disseminate this dissertation /

thesis in print or electronic format for academic / research purpose.

Date:

Place: (DR. SHIVALEELA M.KUDARI)

© Rajiv Gandhi University of Health Sciences, Karnataka.

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ACKNOWLEDGEMENT

I express my deep sense of gratitude to their great holiness Shri Jagadguru

Abhinava Shivananda Mahaswamiji for their divine blessings.

I express my sincere gratitude to the Principal Dr. G.B. Patil and management

committee for giving me the opportunity to pursue my post graduation studies in this

institution.

I express my deep sense of gratitude to my respected parents Smt. Sushila & Late

Shri Mallikarjun. S. Kudari, who filled the inner strength to me to achieve every mile

stone in my life.

I express my deep sense of gratitude to Dr. G.V. Mulgund MD (Ayu) (H.O.D), Dept

of Post graduate studies and Research in Dravyaguna, D.G.M.A.M.C Gadag. He has been

very kind to guide me in research and for whose extraordinary efforts and most valuable

advice made me to complete this work.

I would like to express my profound gratitude and extremely thankful to my guide

Dr. Kuber Sankh MD (Ayu) Professor Dept. of Post Graduate studies and Research in

Dravyaguna, D.G.M.A.M.C Gadag for his inspiring paramount thoughts, Zealous

suggestions, tremendous encouragement and most valuable guidance rendered for the

successful completion of this research work.

I express my sincere gratitude to Dr.Shashikant.B. Nidagundi M.D. (Ayu) Lecturer

Post graduate studies and Research in Dravyaguna, DGMAMC Gadag his most valuable

guidance and inspiration made me for the successful completion of this research work.

I Express my deep sense of gratitude to Dr. G.S. Hiremath M.D. (Ayu) PGARC

D.G.M.A.M.C. Gadag their most valuable guidance, inspiration & constant co-operation

at various stages of my research work.

I express my sincere thanks to Dr. Santosh Belavadi Lecturer, Dept. of

Panchakarma Post graduate studies D.G.M.A.M.C Gadag for their valuable guidance and

inspiration given at different stages of my work.

I am thankful to Shri. Shivakumar Inamadar Lecturer, K.L.E.’S College

Pharmacy Gadag, Shri Suresh Hiremath, Bhoomannavar Madam, Lecturer Dept of

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Pharmacognosy & Shri Anant Bhandarkar Lecturer, K.L.E’s College of Pharmacy Hubli.

For their timely guidance & Help.

I express my sincere gratitude to Dr. U.V. Purad. H.O.D. Dept of Roganidana,

D.G.M.A.M.C. Gadag for their encouragement during the course of the study.

I am very much thankful to Deepa madam, Girish sir, Dept of Biotechnology for

their help in Phyto chemical analysis. I am very much thankful to Shri Nandakumar sir

for his help in statistical analysis of results.

I wish to convey thanks to my respected HOD’s of other Dept. Dr. M.C. Patil,

Dr. V.V. Vardacharyalu, Dr. Purushottamacharyalu, and Lecturers Dr.K.S.R. Prasad,

Dr. R.V. Shettar, Dr. Shivaramadu, Dr. Suresh Babu, Dr. K.S. Paraddi, Dr. Rajashekar,

Dr. Girish Danappagoudar, Dr. Shashidhar Doddamani, Dr. Jagadeesh Mitti, Dr.

Mulkipatil, Dr. Yasmin, Phaniband, Dr. Veena Kori, Dr. Samudri, & Dr. Shankargouda.

I am very much thankful to Dr. Annapurna & Dr Siddhalingesh. M. Kudari,

Lecturer B.V.V.S. Bagalakot for supporting me in preparing the dissertation right from

beginning to end.

I sincerely thank my beloved seniors Dr. K.S. Hiremath, Dr. Bani, Dr. Sajjanar,

Dr. Bingi, Dr. Sunitha. G. Dr. Jagadeesh Handiganur, Dr. Gangoor, Dr. C.B. Inamadar,

Dr. Doddamani, and special thanks to my classmates Dr. V.M. Katarki, Dr. Ashwini

Vastrad, Dr. Shalini Sharma, Dr. Rudrakshi, Dr. Suma, Dr. Jayashree, Dr. Kattimani, Dr.

Shivaleela Kalyani, Dr. Kamalakshi, Dr. Ashok, Dr. Sulochana, Dr. Madhushree, Dr.

Payapgoudar, Dr. Budi, Dr. Prasanna, Dr. Shiba,

I am thankful to junior friends Dr. Jaya, Dr. Savita, Dr. Kalavathi, Dr. Mukta,

Dr. Sevantika, Dr. Asha, Dr. Hiremath, Dr. Bhupesh, and other PG Department Seniors

and Juniors for their constant co-operation and help.

It is my privilege to express my gratitude & affection to my sisters Sarvamangala,

Savita, Jayashree & the respected Jijajis Shivabasav sobarad, Jayashubh Manvi, Suresh

Deshanur for their blessings to me in each and every step of my education & also who

filled the inner strength to me to achieve mile stone in my life.

I am highly indebted to my mother -in –law Smt. Lalita & Father-in-law

Fakkeerappa Hullur, for their co-operation and Help.

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I express great love towards my daughter spurti who has inspired me by her

cuteness and naughty activities.

I wish to convey my thanks to beloved librarian Shri. V.M. Mundinamani, Kerur,

Sureban and Shavi for providing me essential references in the study.

I am very much greatful to all lecturers house surgeons, Hospital staff and non

teaching staff for their timely assistance in completion of this work.

I am whole heartedly very greatful & dedicate this Dissertation work to my

respected Husband Mr. Siddhalingesh Hullur, and my daughter Spurti the prime

reasons for all my success.

Finally I thank God for making all those wonderful people happen to me & pray

for continued blessing and success.

Date:

Place: Dr. Shivaleela .M. Kudari

iii

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ABBREVIATIONS

A. H. - Ashtanga Hridaya

A, K. - Amara kosha

A.P.I. - Ayurveda Pharmacopoea of India

Ab.R - Abhidhana Ratnamala

A. S - Ashtanga sangraha

B. N - Bhavaprakasha Nighantu

B. S - Bhela samhita

C. S - Charaka samhita

D. N - Dhanvantari Nighantu

D. G - Dravya Guna by P.V.Sharma

I.M.P - Indian Medicinal plants

K. N - Kaiyadeva Nighantu

K. S - Kashyapa samhita

Md.G - Madhava Dravyaguna

M. N - Madhava Nidana

Mh. N - Mahoushadha Nighantu

N. A - Nigantu Adarsha

R.N. - Raja Nighantu

S.S. - Sushruta Samita

Sha.S - Sharangaradhara Samhita

Sh. N. - Shaligrama Nighantu

V.S. - Vangasena

V.N. - Vanoushadhi Nidarshika

Y.R. - Yogaratnakar

iv

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ABSTRACT

Background

Health and disease are the two faces of a coin. Ayurveda is the safest curative

system, The concept is to aid the human beings to provide healthy life and to prevent

diseases.

Inflammation can be correlated to shotha on the basis of equivalent symptoms

mentioned in the concerned literature. Inflammation is a symptom according to modern

system while Ayurveda signified it as a disease in accordance to shotha.

Inflammation is a common pathological condition, neither limited to age group

nor socio economical class of society.

Ayurvedic management measures seem to be more satisfactory, because of their

simplicity, applicability and easy availability and cost effectively.

Here the effect of Devadaru (Cedrus deodara) as shothahara (Anti-inflammatory)

has been carried out Devadaru has been mentioned as shothahara in all the Brahatrayees.

In this study Alcoholic extract and Aqueous extract of Devadaru has been taken

as test drug. They are compared with standard and control group with respective

parameters.

Objectives

1) Preliminary Phytochemical investigation of Devadaru[Cedrus deodara].

2) To evaluate the shothahara (anti-inflammatory] effect of Devadaru by

carrageenan induced Albino rats in four different groups.

3) To compare the shothahara effect of aqueous and Alcoholic extract of Devadaru

along with control and standard drug treated groups.

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Method

In this experimental study randomly 24 rats are selected, made 4 groups & 6 rats

in each group, group I serves as control – Normal saline, Group II standard – Ibuprofen,

Group III – Aqueous extract of Devadaru, Group IV – Alcoholic extract of devadaru.

Inflammation is to be produced in to the sub plantar region of left hind paw of all

the rats with 0.1 ml carrageenan, the paw volume of each rat is measured with the help of

plethysmograph, after half, one, two and three hours.

Results

Both 3rd and 4th Group showed significant results but 4th group showed more

significant than 3rd.

Conclusion

In this experimental study the alcoholic extract of Devadaru has shown highly

significant anti inflammatory activity.

Key words

Shotha, Anti-inflammatory, Devadaru, Albino rats, Carrageenan, Plethysmograph.

vi

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CONTENTS

Page No

1. Introduction 1-3

2. Objectives 4

3. Review of literature

A) Drug Review 5-17

B) Disease Review 18-60

4. Methodology 61-70

5. Results 71-96

6. Discussion 97-101

7. Conclusion 102-103

8. Summary 104-105

9. Bibliography 106-116

10. Annexure 117

11. Photographs

vii

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LIST OF TABLES Table 1 DEVADARU

Page No.

Table 1.1 – Showing Gana and Varga according to different authors 05

Table 1.2 – Showing synonyms according to different authors 06

Table 1.3 – Showing Guna according to different authors 12

Table 1.4 – Showing Karma according to different authors 13

Table 1.5 – Showing Prayojy anga according to different authors 13

Table 1.6 – Showing Prayoga according different authors 14

Table 1.7 – Showing Matra according different authors 15

Table 2 DISEASE

Table 2.1- Showing Nidana of shotha according to different authors 21

Table 2.2 – Showing Purvarupa of shotha according to different authors 24

Table 2.3 – Showing Samanya lakshana of shotha according to different authors 25

Table 2.4 – Showing Lakshana of vataja shotha according to different authors 25

Table 2.5 – Showing Lakshana of pittaja shotha according to different authors 26

Table 2.6 – Showing Lakshana of kaphaja shotha according to different authors 26

Table 2.7 – Showing Lakshana of dvidoshoja shotha according to different

authors 27

Table 2.8 – Showing Lakshana of sannipataja shotha according to different

authors 27

Table 2.9 – Showing Lakshana of raktaja shotha according to different authors 28

viii

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Table 2.10 – Showing Lakshana of Abhighataja shotha according to different

Authors 28

Table 2.11 – Showing Lakshana of vishaja shotha according to different authors 29

Table 2.12 – Difference between Acute and chronic inflammation 40

Table3 METHODOLOGY

Page No

Table 3.1- Showing Protocol of the experimental study 69

Table 3.2- Showing concentration and doses before induction of inflamation 69

Table 4 OBSERVATIONS AND RESULTS

Table No 4.1- showing the Phytochemical investigation of Devadaru 75

Table No: 4.2 showing Physico chemical values of Devadaru 76

Table No: 4.3 Results of Parameter 1st of all groups 81

Table No: 4.4 Summary of data of parameter 1st of all groupss 81

Table No: 4.5 ANOVA table for Parameter 1st between groups 81

Table No: 4.6 Comparison for Parameter 1st between the groups 81

Table No: 4.7 Results of Parameter 2nd of all groups 84

Table No: 4.8 Summary of data of parameter 2nd of all groups 84

Table No: 4.9 ANOVA table for Parameter 2nd between groups 84

Table No: 4.10 Comparison for Parameter 2nd between the groups 84

Table No: 4.11 Results of Parameter 3rd of all groups 87

Table No: 4.12 Summary of data of parameter 3rd of all groups 87

ix

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Table No: 4.13 ANOVA table for Parameter 3rd between groups 87

Table No: 4.14 Comparison for Parameter 3rd between the groups 87

Table No: 4.15 Results of Parameter 4th of all groups 90

Table No: 4.16 Summary of data of parameter 4th of all groups 90

Table No: 4.17 ANOVA table for Parameter 4th between groups 90

Table No: 4.18 Comparison for Parameter 4th between the groups 90

Table No: 4.19 The mean of all the groups for all the parameters 93

LIST OF GRAPHS

Graph 1- Paw volume observed in individual rat of control group after 30 min 82

Graph 2- Paw volume observed in individual rat of standard group after 30 min 82

Graph 3- Paw volume observed in individual rat of trial group A (Aq extract)

after 30 min 83

Graph 4- Paw volume observed in individual rat of trial group B (Alc extract)

after 30 min 83

Graph 5- Paw volume observed in individual rat of control group after 1 hr 85

Graph 6- Paw volume observed in individual rat of standard group after 1 hr 85

Graph 7- Paw volume observed in individual rat of trial group A (Aq extract)

after 1 hr 86

Graph 8- Paw volume observed in individual rat of trial group B (Alc extract)

after 1 hr 86

Graph 9- Paw volume observed in individual rat of control group after 2 hrs 88

Graph 10- Paw volume observed in individual rat of standard group after 2 hrs 88

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Graph 11- Paw volume observed in individual rat of trial group A (Aq extract)

after 2 hrs 89

Graph 12- Paw volume observed in individual rat of trial group B (Alc extract)

after 2 hrs 89

Graph 13- Paw volume observed in individual rat of control group after 3 hrs 91

Graph 14- Paw volume observed in individual rat of standard group after 3 hrs 91

Graph 15- Paw volume observed in individual rat of trial group A (Aq extract)

after 3 hrs 92

Graph 16- Paw volume observed in individual rat of trial group B (Alc extract)

after 3 hrs 92

Graph 17- Mean Paw volume of all group after ½ hr 93

Graph 18- Mean Paw volume of all group after 1 hr 94

Graph 19- Mean Paw volume of all group after 2 hrs 94

Graph 20- Mean Paw volume of all group after 3 hrs 95

MASTER CHART

1. Showing Assessment of Parameters I, II, III & IV of all groups 80

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LIST OF PHOTOGRAPHS

SL.No Name of the Photograph

1. Devadaru Tree

2. Stem bark of Devadaru

3. Aqueous extraction

4. Alcoholic extraction

5. Evaporation over hot plate

6. Aqueous extract & Alcoholic extract

7. Phyto chemical analysis

8. TLC Plate

9. Rats in cage

10. Oral administration of the drug.

11. Injecting carrageenan to left hind paw of rat.

12. Left hind paw Albino rat after inducing inflammation.

13. Measurement of inflammation using plethysmograph.

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Introduction

INTRODUCTION

Ayurveda is a science of life with two main objectives maintenance and

promotion of positive health and cure of the diseases. Ayurveda is believed to be

prevalent since 5000 years in India. In 1974 w.h.o. recognized Ayurveda the Indian

traditional medicine and requested to improve the service and availability of

ayurvedic drugs in our country. This traditional medicine is much popular for curing

the most of the diseases.

Among the countless number of ailments in this world a few can be identified

as very common and recurrently affecting, where inflammation is also one of those.

Inflammation is mentioned in modern system of medicine as a symptom rather than a

disease. Ayurvedic references have showed it is a disease entity by explaining the

following Samprapti in other word the Pathogenesis.

“Vatadosha undergoing increase, pushes out the increased Rakta, pitta, and

kapha to exterior (twak) by blocking their channels and produces swelling of skin and

muscles (twak, mamsa). It is called Utseda, Samhata, Shotha in view of increased

size.” (Ma.Ni.36th chapter). It is an important entity and has a nearer meaning to the

kind of inflammation.

It is believed that every dravya available on this earth has medicinal property

in it; only thing should be used rationally. Further more it is said that even a poison

can be good medicament if used with caution.

In Ayurvedic texts inflammation has been described under various terms like

Shotha, Shopha, Shwayatu, Vrana shotha. But the term shotha is used specially for

inflammatory swelling.

It is self protective reaction of the tissue towards infection, irritants or foreign

substances. Though it is a part of host defense mechanism when it becomes great it

Anti Inflammatory effect of Devadaru 1

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Introduction

turns to be a hopeless condition, which cause tissue damage. Similarly the

exaggerated inflammatory reaction also do harm to the body. Therefore the timing of

inflammation is essential.

It is also oftenly associated with changes that affect the body as a whole in

particular with leucocytosis and pyrexia. Inflammatory process involves a series of

events that can be elicited by numerous stimuli (infection, antigen antibody reaction,

physical or thermal injuries) efforts to control shotha or inflammation where the time

of Sushruta. Its importance and vastness can be well understood by the voluminous

work done by him on this subject. He has dealt with this entity efficiently from

different angles and described a range of ganas in detail to treat shotha. Not only

Sushruta even Charaka has also mentioned Shothahara dravyas and its ganas along

with various measures to deal with it.

Anti-inflammatory drugs of modern medicine are affective but have number of

side effects causing gastric erosion, haemorrhage etc. Inflammatory drugs are

classified

Non-Steroidal Anti-Inflammatory Drugs (NSAID)

Steroidal Types.

The chemicals which are comes under this headings can produce undesired

effect in therapeutic usage includes interstitial nephritis, hepatic cell damage, fluid

retention, skin rashes etc. By continuous usage of steroids will disturb the

physiological system and causes the multiple complications. To combat these

problems it is necessary to evaluate plant based anti-inflammatory agents.

There are many inflammatory drugs described in AYURVEDIC Literature,

among them Devadaru [Cedrus deodara] is one of the most potent anti inflammatory

drug, .

Anti Inflammatory effect of Devadaru 2

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Introduction

Devadaru [Cedrus deodara] is the big tree of family pinaceae mainly found in north

western Himalayas, having the properties like, tikta rasa laghu snigda guna, ushna

veerya, katu vipaka, acts as kaphavata shamaka and indicated in vibandha, admana,

shotha, ama tandra, hikka, jwara, rakta dosha, prameha,peenasa, kaphaja kasa and

kandu.

The parts used in this drug are kashta and taila. The major chemical constituents of

essential from wood are P-methyl aceto phenone, sesquiterpenes, stembark cotains

deodarin,toxifolin. Its local application and oil are used in arthritis, its oil is very good

wound cleaner and healer.

In present study an attempt is made to preliminary phytochemical investigation of

cedrus deodara extraction were conducted and observed the presence or absence of

alkaloids, proteins, carbohydrates, steroids, saponins, tannins, resin, starch, oils, and

fats and TLC methods were done. During experimental study total 24 albino rats were

taken and subjected them in four groups [Group I to IV]. Group I was control group.

Group II was standard group, Group III was Trial Group A with Aqueous extract and

group IV was Trial group B with Alcoholic extract, After induction of carrageenan

immediately inflammation was observed and measerd then compared the

sthothahara[anti inflammatory] effect of aqueous extract and alcoholic extract of

Devadaru along with control and standard drug treated groups.

Anti Inflammatory effect of Devadaru 3

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Objectives

OBJECTIVES OF THE STUDY :

1. Preliminary Phytochemical investigation of Devadaru (Cedrus deodara)

Extraction

Chemical analysis - Test for alkaloids, flavonoids, triterpenoids,

glycosides, steroids, saponins, tannin, carbohydrate, proteins, resin,

starch, oils and fats.

Thin layer chromatography (TLC)

2. To evaluate the shothahara (anti inflammatory) effect of Devadaru by

carrageenan induced paw oedema method14 .

3. To compare the shothahara (anti inflammatory) effect of aqueous extract

and alcoholic extract of Devadaru along with control and standard drug

treated groups.

Anti Inflammatory effect of Devadaru 4

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Drug review

DRUG REVIEW

Historical aspect of the Drug (Drug)1

In Parasara grhya sutras and kousika sutras we come across the references

about Devadaru (P.G.S. 1/19 & Kou, su 58/16). Panini also quoted regarding

Devadaru vanam (P.M. 8/4/18).

Table No. 1.1 Ganas and vargas according to different classics.

Charaka samhita Stanya shodhana

Anuva sanopaga

Katukaskandha

Sushruta samhita Vata samshamana

Eladi gana

Rakta sravaka varga

Astanga hriday Niruhana varga

Vata samshamana varga

Vachadi varga

Eladi varga

Bhavaprakasha Nighantu Karporadi varga

Nighantu Adarsha Devadarvadi varga

Kaiyadev Nighantu Aushadhi varga

Raj Nighantu Chandanadi varga

Dhanvanatari Nighantu Guduchyadi varga

Madanapala Nighantu Abhayadi varga

Shaligram Nighantu Kapooradi varga

Abhidana Ratnamal Tikta dravya skanda

Madhava dravya guna Vividoushadhi varga

Amara kosha Vanoushadi varga

Anti Inflammatory effect of Devadaru 5

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Drug review

Table No. 1.2 Paryayas according to different authors

Synonyms C2 S

S3 S

A4 H

B5 N

K6 N

R7 N

D8 N

M9 N

N10 A

Ab11 R

A12

K S13

N M14

N Indradaru - - - + - - - - - - + - - Masta daru - - - + - - - - - - - - - Drukilima - - - + - - - - - - - - - Kilima - - - + + - + - + - - + + Darubhadra - - - + - - - - + - - + - Surabhuruha - - - + - - - - - + - - - Surahva - - - - + - + + - - - - - Snehaviddha - - - - - - + - - - - - - Mahadaru - - - - - - + - - - - - - Bhadradaru - - - - + + + + + - - + + Devakashta - - - - + - + - - - - - - Puthikashta - - - - - - + - + - - + - Sudaru - - - - - - + - - - - - - Suradaru - - - - - - + - - - - + - Indravruksha - - - - - - + - - - - + - Amaradaru - - - - - + + - - - - + - Suradruma - - - - + - - + - - - + - Bhadrakashta - - - - + - - + - - - - - Snehavruksha - - - - - - - + - - - + - Krimila - - - - - - - + - - - - - Shakradaru - - - - - - - + - - - - - Daruka - - - + - - - - - - - - - Snigdadaru - - - - - + - - - - - + - Shivadaru - - - - - + - - - - - + - Shambhava - - - - - + - - - - - + - Bhutahari - - - - - + - - - - - + - Bhavadaru - - - - - + - - - - - + - Rudradaru - - - - - + - - - - - - - Shakadru - - - - + - - - + - + + - Peetadru - - - - - - - - + - - - - Shakrapadapa - - - - - - - - + - - + - Paribhadraka - - - - - - - - + - - + - Peetadaru - - - - - - - - - - - + - Surahvaya - - - - - - - - - - - + - Bhadravat - - - - - - - - - - - + - Shatapadapa - - - - - - - - - - - + - Kalpapadapa - - - - - - - - - - - + - Daruka - - - - - - - - - - - + - Surakashta - - - - - - - - - - - + - Devadaru + + + + + + + + + + + + + Daru + + + + + - + - + - +

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Paryayas and its meanings15

1. SåuÉSÉÂ : Himalaya isGod’s country where this tree is grown

(V.M.G)

2. pÉSìSÉÂ : Good Fragrant wood (V.M.G)

3. xÉÑUpÉÔÂWû : The tree which grows in God’s country (P.V.S)

4. mÉÏiÉSìÓ : mÉÏiɶÉÉ SìÓÓ¶ÉåÌiÉ | mÉÏrÉiÉå cɤÉÑwÉÉÅrÉqÉç CìÌiÉ | (N.A)

Its kashta is yellow in colour. Its beauty is perceived

through the eyes.

5. mÉÔÌiÉMüɸ : mÉÔiÉå: mÉÉuÉlÉxrÉ MüɸqÉç CìÌiÉ | (N.A)

Its kashta iradicates bad smell.

6. mÉÉËUpÉSìMü : mÉËUÌlɹÉmÉëÉmiÉÇ pÉSìqÉ AxrÉ mÉÉËUqÉSì: |

mÉÉËU ÌlÉ¹Ç mÉëÉmiÉ pÉSìèqÉxrÉåÌiÉ | (N.A)

Its sevana causes paripurna kalyana

7. zÉ¢ümÉÉSmÉ : zÉ¢üxrÉ CuSìxrÉ mÉÉSmÉ: uÉפÉ: CìÌiÉ |

This is the tree of Indra

8. pÉSìSÉ : pÉSìÇ SÉ CìÌiÉ | (N.A)

Its kashta is best among all the kashtas.

9. ÌMüÍsÉqÉ : ÌMüsÉÌiÉ ¢üÏQûÌiÉ sÉbÉÑiuÉÉiÉç | (N.A)

Beacause of its light weight moves freely.

10. mÉÏiÉSÉ : mÉÏiÉÇ cÉ iÉSèSÉ cÉ CÌiÉ, mÉÏiÉÇ SÉÂxrÉåÌiÉ uÉÉ |

Its Kashta is having peetavarna (N.A)

11. SåuÉSÉ : SåuÉÉlÉÉÇ SÉ CìÌiÉ; SÉÂhÉÉÇ uÉÉ SåuÉ: CìÌiÉ; (N.A)

Its kashta resembles God so it is shreshta.

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12. SÉ : SÉUrÉÌiÉ ÌuÉoÉlkÉÉÌS UÉåaÉÉlÉç CìÌiÉ | (N.A)

It iradicates vibandhadi rogas.

13. mÉÔÌiÉMüɹ : mÉÔÌiÉ EaÉëaÉÇlkÉ MüɹqÉç AxrÉ CìÌiÉ | (N.A)

Its kashta is having Ugragandha.

Vividha Bhasha naam (Vernacular Names)

Latin Name : Cedrus deodara

Sanskrit : Devadaru, Badradaru, Suradaru, Snehavidda, Vrika

shapa.

Hindi : Devadar, Deodar, Toona

Marathi : Devadar

Gujarathi : Devadar

Telagu : Devadari

Kannada : Devadar

Bengali : Devadaru, Toon

English : Deodar, Pinus Deodara, Himalayan cedar.

Tamil : Toon – maram, Devadaru

Malayalam : Devadaru

Punjabi : Pahari – keli

Arabic : Sanobarulhind, Shajratudde vadar

French : Deodar

Afghanistan : Imanza, Nikhtar

Garhwal : Dadar, Deodar, dewadar, Diar

Kashmir : Dadar, Dar, deodar.

Urdu : Deodara

Himalaya : Kalu, Keoli, Kilar Kilei.

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Botanical Classification

Kingdom Plantae

Sub Kingdom Tracheobionta

Division Coniferophyta

Class Pinopsida

Order Pinales

Family Coniferae

Genus Cedrus

Species Deodara

Family 16

Kula : Devadaru kula

Family : Coniferae

CONIFERAE

Trees or shrubs, usually resinous, mostly evergreen. Leaves usually needle-

like or scale-like, rarely with a broad blade; stipules 0. Flowers monoecious or

dioecious, perianth 0. Male flowers in deciduous catkins consisting of stamens which

are usually scale- like and bear 2-6, rarely more, 1-celled pollen-sacs on the lower

surface. Female flowers in cones, consisting of scale-like open carpels which are flat

or peltate and bear either directly or on a special subsidiary scale (placental scale) 1-2

many ovules or the female cone reduced to a single ovuliferous scale or to a single

ovule. Fruit usually a woody cone sometimes berry-like or formed from the ovule

alone in which case the outer coat usually becomes fleshy. Embryo with 2-16

cotyledons.- Throughout the world, chiefly in cold regions.

A. Scales of the female cone opposite, in several series. Leaves Very short of subulate

1. Scales of cone woody; testa winged …………………. Cupressus.

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2. Scales of cone cohering into a globose berry-like fruit enclosing the seeds;

testa hard not winged…………. Juniperus.

B. Scales of female cone or spike few. Leaves scattered or bifarious

1. Leaves persistent, in bundles of 2,3 or 5, narrowly linear.

Scales of cone persistent……………………………. Pinus.

2. Leaves persistent, in bundles of many, acicular, scales of erect cone deciduous

…….. Cedrus.

3. Leaves more or less distichous, linear. Scales of large erect cone deciduous

.The bark and leaves are astringent; the resin and the essential oil are

stimulant, diuretic, and anthelmintic.

The glucoside coniferin occurs in the cambium sap of coniferous trees; thujin

occurs in Thuya.

A toxic alkaloid, taxine, has been isolated from the leaves, shoots, and fruits of

the yew. Other toxic substances obtained from members of this order are formic

acid, oil of savin, oil of yew.

Swaroop (Botanical Descriptions)17

A large evergreen tree of height 85 mtrs.

Kanda (Stem) : Big erect having circumference 12 mtrs.

Twak (Bark) : Thick and cracked.

Patra (leaves) : are green, elongated with tapering ends.

Pushpa (Flowers) : Green, Yellow and appear in clusters.

Phala (Fruit) : Ripe fruit is black having seed 1 cm. Long

The tree bears new fruits in October, which ripe within a year.

Deodar true has a long life having life span of 600 years.

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Botanical description according to modern18

Cedrus deodara is a large evergreen tree. It grows up to the height of 250 feet.

Branches – Not whorled the leading shoot and tips of the branches usually drooping.

Bark – Dark sometimes almost black usually very rough on oil stems, some time only

lightly furrowed.

Stem – Straight and wide usually of 36 feet circumference, The branches at the above

are small sequence, From far away it looks like a triangle shape.

Shoots – Dimorphic, long shoots with the needles solitary and arranged spirally.

Leaves – 2.5 – 3.8 cm long, needle like, triquetrous, sharp pointed.

Flowers – Usually monoecious, but some tree or branches habitually bears flower of

one sex, male catkins solitary at the end of the branches, Female flowers in cones,

which are solitary at the end of branches.

Fruits – are 4-5 inches long and 3-4 inches breadth & raised. The apex is rounded and

has many scales, its edges are thin.

Seeds – are 7.5 15mm long, pale brown wing longer, then the seeds are triangular in

shape and sides are rounded.

The fruits occur in October month and ripe in 1 year. The age of devadaru is generally

600 years.

Habitat19

Devadaru grows mainly in North-westernHimalayas from Kashmir to Garhwal.

Forests of Deodar found in Kashmir, kulu, chamba, Tehri – Garhwal,simla, Almora

and Mussoorie hill stations.

Bedha according to different authors:

According to Raj Nighantu & Shaligram Nighantu20,21

Snigdadaru, Kashta daru

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Snigda daru – It has thick and oily wood & available in the market in the name of

‘Dhoopa’

Kashta daru – Ashoka tree is known as kashtadaru the leaves of this tree are used for

festive occasional its latin name is Polyalthia longifdia, Anonaceal family i.e

sitaphalakula.

Table 1.3 Gunas (Properties) According to different author.

Properties B22

N

D23

N

M24

N

R25

N

K26

N

N27

A

S28

N

Vanoushadhi29

Nidarshika

P.V. Sharma30

Rasa

Tikta + + + + + + + + +

Katu - - + - + - - - -

Guna

Laghu + - - - + - + + +

Snigda + + + + + + + + +

Veerya

Ushna + + + + + + + + +

Vipak

Katu + - + - + + + + +

Doshaghnata

Vatahara + + + + + + + + +

Kaphahara + + + + + + + + +

Chemical Composition

Wood oil contains oleo-resin, essential oil, and needles (leaves) contain

ascorbic acid. Essential oil from wood: Premethylacetophenone, atlantone,

sesquiterpenes (α&β himochalene, himachalol etc); stem bark: deodarin, toxifdin 31.

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Table 1.4 Karmas according to different authors.

Karmas C32

S

S33

S

A34

H

BP35

N

D36

N

R37

N

K38

N

N39

A

RS40

A

M41

N

P.V.S42 Van

Dar43

Shothahara + + + + + + + + + + + +

Karnashoolahara - + - - - + - - - - + +

Hikkanigrahana + - - - + - - - - - + +

Varnashodhana - + - - - - - - - - + +

Vrana ropana - + - - - - - - - - + +

Rakta prasadana - - + - - - - - - - + -

Deepana - - - - - - - - - + + +

Pachana - - - - - - - - - + + +

Krimighna - - + - - - - - - - + -

Anulomana + + + + - + - - + - + -

Swedajanana - - - + - - - + - - - -

Vedanastapana + + + + - + - - - - + +

Kandughna - - - + - - + - - - + +

Mutrajanana - - - - - - - - - - + +

Stanyashodana - - - + - + - + + - + +

Jwaraghna - - - - - - - - - - + +

Lekhana - - - - - - - - - - + +

Rasayana - - - + - - - - - - - -

Amapachaka - - - + + + - - - - + +

Hridayattejaka - - - - - - - - - - + +

Kushtaghna - - - - - - - - - - + +

Pramehaghna - - - + - - - - - - + +

Table 1.5 Prayojya anga

Part used DG44 P.V.S

R45 N

B46

N N47

A Pharmacopoea48

indica DG49 V.M.G

Van Dar50

Kashtasara + + + + - + + Taila + + + + + + + Bark - - - - + - -

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Table No. 1.6 Prayoga according to different authors.

Prayoga C51

S

S52

S

A53

H

BP54

N

K55

N

R56

N

M57

N

D58

N

N59

A

S60

N

D.G

P.V.S61

D.G62

J.L.N

Vibandha - - - + + + - + - - + -

Admana - - - + + + + + - - + +

Shotha + + + + + - + - + + + +

Tandra - - - + - - - - - - - -

Hikka + - - + + - + - + - + +

Jwara - + - + + + + - + + + +

Prameha - - - + + + - +` - - + +

Peenasa - - - + + - - - + - - +

Kasa - - + + + - - - + - + +

Kandu - - - + + - + - - - + +

Amavata - - - + + - + - - - + +

Shirahashula - - - + - - - - - - - -

Shleepada - - - + - - - - - - + -

Jalodara - - - + - - - - - - - -

Shwasa + - - + + - - - + + + +

Atisara - - - + - - - - - - + -

Ashmari - - - + - - - - - - + -

Vrana - - - + - - - - - - + -

Kushta - - - + - - - - - + + +

Karnashoola - - - + - - - - - - - -

Raktavikara - - - + + - - - - - + -

Aaamavikara - - - - - + - + - + + -

Arsha - - - - - + - - - - + -

Bhootabadha - - - - - + - - - - - -

Vruna - - - - - - - - - + - +

Shleepada - - - - - - - - + - - -

Kushta - - - + + - - - + + + -

Karnashoola - + - - - - - - + - + -

Krimi - - + - - - - - + - + -

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Action and uses in other system of medicine63

Unani – Hot 2, Dry 2, Resolves inflammation, antispasmodic, anti-poison, paralysis,

stone in the kidney, fevers.

Oil: Hot - 20, Dry – 10, for injuries (external).

Action:

Wood is carminative, bark is powerfully astringent and febrifuge. Leaves have

mild terebinthinate properties.

Uses:

Bark is a good remedy in remittent and intermittent fevers, diarrhoea and

dysentery and though not bitter it is a fair substitute for perurian bark particularly

when united with powdered Bonduc nut. Its powder is applied with much benefit in

the treatment of ulcers. It is considered especially useful in bilious fevers and

inveterate diarrhoea arising from atony of the muscular fibre.

Oleo-resin and dark coloured oil or turpentine, are applied to ulcers and skin

diseases. They are valuable in manage in horses and sore feet of cattle.

Controverisial studies64

Thakuriji is of the opinion that pinus species such as P excelas wall and even

P. Longifolia Roxb are known as kaila and kolaina respectively at Garhwal, It is

therefore, possible that kilima supposed to be synoym of Devadaru by charaka may be

a varity of sarala.

Table 1.7 Matra (Posology)

D.G65

P.V.S

D.G66

Hastamalaka

D.G 67

(V.M. Gogle)

Powder 3-6 gm 1-3 gm 1-3 Gm

Oil 20-40 drops 10-20 drops 20-40 drops

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Therapeutic uses 68

Charaka – Hikka & Shwasa – The decoction of Devadaru should be given

(Ch.Chi, 21-112)

Sushrut -= Jwara – Decoction of devadaru is given

Shotha – Decoction of devadaru is given with Gomutra is givens.

Vagbhata – Kaphajakasa – The cloth which is dipped in the oil should be roll over

the cedar wood and burnt while burning the oil drops

comes from it, To this oil, yavakshara & Trikatu are

mixed The preparation destroys kaphaja kasa.

Hareeta – Vatajanya vruna – Devadaru & Shunti are rubbed & the paste is applied

over the wound.

Chakradatta – Shleepada – Chitraka moola & Devadaru oil are powdered & mixed

with Gomutra, then by applying the paste it gets relief.

Vangasena – Kaphajanya Gandamala – Devadaru and Indravaruni moola are

pasted with water & applied.

Shleepada – Devadaru choorna with sarshapa taila is given.

Shodhala – Kushta – By burning Devadaru moola one type of Rasa will get if it is

taken with dugda all types kushta will iradicate.

Karnashoola – The cloth which is dipped in the oil is roled over the cedar wood &

burnt by burning one type of Rasa or Taila is extracted. This taila

relieves karna shoola.

Pilla namaka Netra roga – To Devadaru sukshma choorna Ajamutra bhavana is

given then it is used as Anjana for netra roga.

Rasahrudaya tantra – Peenasa – Devadaru taila with Goghrita is given.

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Formalutions of Devadaru

• Devadarvyadi kwatha

• Devadarvadi choorna

• Devadarvadyarishta

• Rasanadi kwatha

• Satyadi choorna

• Karanjadi yoga

• Rasana panchak kwatha

• Punarnavadi mandoora

• Vishagarbha taila

• Chandra prabha vati

Research Works69

• The alcoholic extract of the stem was found to have anticancer activity against

human epidermal carcinoma of the nasopharynx in tissue culture ( 1968).

• Stem bark etxtract showed significant anti-inflammatory activity in

rat.(Ind.J.Pharmacol 1973).

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DESEASE REVIEW

SHOTHA (SHOPHA)

NIRUKTI

The word shotha is derived from the root “Savagathou Bahulakath Pha” which

means instantly spreading.

“Shwayathu” is derived from the root word “Do aswigativridyah” which means by shich

the body is bulging70.

When AjÉÑcÉ mÉëirÉrÉ is added to the aÉÌiÉuÉ×̬AjÉïrÉÑ£ü OÒûAÉåꦃ kÉÉiÉÑ The word shotha is derived71.

“Shotha” “Shwayathu” “Shopha” very marked swelling of the skin on any place is to be

under stood.

PARIBHASHA

Shotha is a disease caused due to the Derangement of Doshas, which may appear

at any part of the body involving Twak and mamsa. It is characterized byswelling, pain,

Redness and raised local temperature.

‘Shotha’ is found as a main symptom in many number of ailments like Granthi,

vidradhi, Alaji etc. But that which is going to spread vastly, which is nodulated, equal or

unequal (Sama or Vishama) and particularly located dosha-samuha in the Twak (skin)

and Mamsadi dhatus (tissue elements) is Shotha72.

NIDANA

Causative factors for endogenous type of Inflammation are as listed below

according to different classical references;

According to Charaka

1. Consumption of kshara (alkaline preparation) amla (Sour food and drinks),

tikshna (articles of food and drinks having sharp attribute), ushna (hot food and

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drinks) and guru (heavy food) by a person who is weak and emaciated because of

shodhana (Elimination therapy of Panchakarma).

2. Intake of curd, uncooked food, mrut (mud) shaka (leafy vegetables), virodhi anna

(Ingredient of food having mutually contradictory properties), dushta anna

(polluted food including water in the beginning of rainy season) or food afflicted

with gara (artificially prepared poison).

3. Afflictions with arsha (piles) and lack of exercise.

4. Administration of elimination therapies in improper time.

5. Irregular delivery including abortion and miscarriage.

6. Inappropriate administration of elimination therapy and improper care of the

patient after the administration of these therapies.

Another opinion of Charaka is- Hardship of the external skin by the Abighatha of

wood, stone, weapon, fire, poison and iron equipments gives leads to prakupita of doshas,

these doshas vitiates twacha gives rise to rise to exogenous type of inflammation.

Similar opinion is expressed by Sushrutha and Vagbhata. Along with all the above

factors Vagbhata adds that - doshas localised in the chest produces inflammation in the

upper part of the body, those prevailing in the region of the urinary bladder, produce

Inflammation in the lower parts of the body, those localized in the middle part produce

inflammation in the middle part of the body; those which are spread all over the body will

produce inflammation of the whole body and localized in any one part will cause

inflammation of that part only.

Nija Shotha Nidana:

Samanya Laxanas include etiogenic factors like- Improper performance of

Pancha Karma; Mithya Samsarjana Krama; Secondary conditions like Chardi (caused by

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Vega Dharana) and Roga janita Karsya. Improper Habits like Upavasa, Vega Dharana,

Ati Guru-Amla- Lavanadhi ahara sevan. Gyneic Factors- Garbhapata (miscarriage), Ama

garbhapatana (abortion); Prajatanam Mithya-apacharat (improper hygiene during

puerperal period).

Vishishtha nidana of Vataja shotha: Ahara- Seeta-Ruksha-Laghu-Vishada

Padarthadi sevanam. Vihara- Shrama, Upavasa, Kshanana.

Vishishtha nidana of Pittaja shotha: Ahara-Ushna-Teekshna-Katu-Kshara-

Lavana-Ajirna Bhojana. Vihara-Agni-Atapa prapata.

Vishishtha nidana of Kaphaja shotha: Ahara- Guru-Madhura-Sheeta-Snigdha

bhojana. Vihara-Ati nidra, Avyayama etc.

Agantuja Shotha Nidanam:

(Injuries: Chedana (excision), Bhedana (cutting), Bhanjana (scalding), Prahar

(beating), Bandhana( tourniquet), Pedana (pressing), Vyadhana (incision) etc., caused by

the sastras (instruments etc.).

Vegetable Sources: Bhallataka, Kapikacchu, Poisonous leaves, Poisonous

climbers /shrubs etc.

Animal Sources : Krimi Suka, Swedana, pari sarpana, Visha pata of poisonous

animals, bite or sting of poisonous animals or the injury caused by the teeth or horns.

Environmental Sources : Sagara vata, Visha Vata, Hima sparsha, Agni sparsa etc.,

factors well known to cause inflammation.

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Table No. 2.1 ÌlÉSÉlÉ

cÉUMü73 xÉÑ´ÉÑiÉ74 uÉÉapÉOû75 1) Improper performance panchakarma 2) Kshara, Amla, Lavana, Tikshna, Ushna, Guru padarta sevana. 3) Apakvanna, Viruddanna, Dooshitaanna, Kritrimavishayukta anna sevana. 4) Affliction by Arsha 5) Vishama prasuti, Garbhapatana, Mudhagarbha 6) Afflication of external skin by the impact of kaasta, ashma, shastra, agni, visha and ayasa implements.

1) Walking after taking the food 2) Guruanna, Shaka, Lavanapradana bhojana, 3) Durbala vyakthi in adhika matra amla padarta sevana, anupa mamsa, ajeerna. 4) Adhika sthree prasanga. 5) Viruddha ahara sevana 6) Riding on horse, camel, chariot,

1) The person who has become week by diseases, therapies, fasting etc, 2) Indulging suddenly in large amount of food or those foods which are guru, amla, snigdha, sheeta, lavana, shara, tiekshna, ushna, shaka, ambu, nidra, ratri jagarana, eating mud, fatigue copulation. 3) Walking long distances holding flags & banners 4) Riding on vehicle and such other strenous acts. 5) Suffering by diseases such as Kasa, Shwasa, Atisara, Chardi, Jwara, Visuchika, Alasaka, Pandu, Visarpa etc.

SAMPRAPTI

According to Charaka:

Charaka has mentioned separate Samprapti for Agantuja and Nija shotha.

Agantuja shotha Samprapti:

The Aganutuja shothas are diagnosed by the characteristic etiology, signs and

symptoms even though ultimately the Agantuja shotha may share the characteristic signs

and symptoms of Nija shotha. The difference lies in the priority or post priority of certain

features common to both type of shotha. The Nija shotha starts with the vitiation of

doshas and then brings about pain. The Agantuja shotha on the other hand starts with pain

and then brings about the vitiation of dosha.

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Nija shotha samprapti

Because of the Nidan-Kapha, Rakta, Pitta enters in the external vessels and

afflicts Vayu localized there, as a result of these factors the passage (channels of

Circulation) get obstructed which spread to nearby areas, thereby causing inflammation.

If these affliction takes place in the chest region, then the inflammation occur in

the upper part of the body (urdhva shotha). If these afflictions takes place in the colon or

pelvic region which is the location of vayu, then the inflammation occurs in the lower

part of the body ( adhah shotha); if these afflictions takes place in the middle part of the

body that is between chest and pelvic region then occurs in the middle part of the body

(Madhya shotha) and if these afflictions takes place all over the body then the

inflammation occurs all over the body (sarvanga shotha) if however these afflictions are

located in any particular viscera, such as throat and palet then inflammation takes place in

that locality and it is designated after the name of the viscera where it occurs (e.g, gala

shotha)76.

According to Vagbhata:

Vata getting increased brings the vitiated pitta, rakta and kapha into the external

channels and getting obstructed by them, produces inflammation localized in the skin and

muscle called utsedha, samhata and shotha77

According to Madhavakara:

Vata undergoing increase pushes out the increased rakta, pitta and kapha to the

exterior (twak skin) by blocking their channels and produces shotha (swelling) of the skin

and muscle (twak mamsa) it is called as Utseda, Samhata and Shotha in view of its

increased size78.

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Schematic representation of Shotha samprapti

Nidana

Vatadosha gets vitiated

Vatadosha vitiates rakta pitta & kapha doshas

Vayumargavarodha

Utsedha

Shotha

BHEDA

According to Charaka79

Even though all the three doshas involved in the manifestation of all the types of

the Shotha, it is on the basis of the predominance of the respective doshas that vataja,

pittaja and kaphaja varieties of disease are determined and therapies are prescribed

accordingly.

All the varieties of the inflammation are considered to be tridoshaja i.e. they are

caused by the vitiation of all the three doshas even so the causes of inflammation differs

from one to another according as the particular dosha which is predominantly vitiated.

The physician should therefore determine the line of treatment according to the

predominance of one dosha or the other.

1) On the basis of Dosha

a) Vataja b) Pittaja c) Kaphaja

2) On the basis of Karana

a) Nija b) Agantuja

3) On the basis of Sthana

a) Ekangaja b) Sarvangaja

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c) - Inflammation pervading the whole body.

- Inflammation pervading the half of the body.

- Inflammation afflicting only one limb of the body.

According to Susrutha80:

As the Shotha develops from the six factors as vata, pitta, kapha, rakta,

sannipatika, agantuja that are the types so called to be the six as Vataja, Pittaja, kaphaja,

Raktaja, Sannipataja and Agantuja .

Depending upon signs, symptoms and treatment earlier six types has been

explained but sarvasara that is the shotha which spread all over the body are of 5 type that

is Vataja, Pittaja, kaphaja, Sannipataja and Vishaja.

According to Vagbhata & Madhavakara81-82:

Based on different causes and symptoms it is of nine types from each dosha

separately, from the combination of two doshas and from the combination of all them,

from trauma/injury and from the poison.

Mainly, it is of two types;

a) Nija, Agantuja

b) Sarvanga, Ekanga

It is known to be of three types

a) Prthu (hard)

b) Unnata (raised/elevated) c) Grathita (glandular) .

PURVA RUPA Table No. 2.2 mÉÔuÉï ÂmÉ

cÉUMü83 xÉÑ´ÉÑiÉ uÉÉapÉOû84

FwqÉÉ SuÉjÉÑ ÍxÉUÉhÉÉqÉÉrÉÉqÉç

---

SuÉjÉÑÈ ÍxÉUÉhÉÉqÉÉrÉÉqÉç AÇaÉ aÉÉæUuÉ

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SAMANYA LAKSHANA

Table No. 2.3 xÉÉqÉÉlrÉsɤÉhÉ

cÉUMü85 xÉÑ´ÉÑiÉ uÉÉapÉOû aÉÉæUuÉ AlÉuÉÎxjÉiÉ EixÉåkÉ FwqÉÉ

ÍxÉUÉiÉlÉÑiuÉÇ sÉÉåqÉWûwÉï ÌuÉuÉhÉïiÉÉ

---

---

VISHESHA LAKSHANA

Table No. 2.4 Vataja shotha:

ÌuÉÍvɹ sɤÉhÉ cÉUMü86 xÉÑ´ÉÑiÉ87 uÉÉapÉOû88 uÉÉiÉeÉ vÉÉåjÉÈ cÉsÉ

iÉlÉÑ iuÉMçü mÉÂwÉ xÉÑÎmiÉ

WûwÉï vÉÉåjÉ (Divabali)

AÂhÉ M×üwhÉ mÉÂwÉ qÉ×SÒ iÉÉåS

cÉsÉ Ã¤É AÂhÉ, M×üwhÉ uÉhÉï MüMïüzÉUÉåqÉrÉÑ£ü xÉlMüÉååcÉ xmÉlSlÉ iÉÉåS Swelling increases and decreases quickly soon spreads to other part of the body Subside by massaging with fatty and hot oil mild at night and severe during day time

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Table No. 2.5 Pittaja Shotha:

cÉUMü89 xÉÑ´ÉÑiÉ90 uÉÉapÉOû91 ÌmɨÉeÉvÉÉåjÉ qÉ×SÒ

xÉaÉlkÉ M×üwhÉ or mÉÏiÉ uÉhÉï pÉëqÉ, euÉU, xuÉåS, iÉ×whÉ, qÉS Tenderness in affected part Eyes becomes red Excessive burning-sensation.

mÉÏiÉuÉhÉïï qÉ×SÒ xÉU£ü AéåwÉ-cÉÉåwÉ-SÉWû Increases rapidly

mÉÏiÉ, U£ü, AÍxÉiÉuÉhÉï qÉ×SÒ xÉaÉlkÉ

accompanied by iÉ×whÉ-SÉWû-euÉU-xuÉåS Desire for cold vÉÏiÉÉæcNûÉ Intolerable to touch Appears first in middle part then spreads throughout body.

Table No. 2.6 Kaphaja Shotha:

cÉUMü92 xÉÑ´ÉÑiÉ93 uÉÉapÉOû94 MüTüeÉ vÉÉåjÉ

aÉÑ vÉÏiÉ ÎxlÉakÉ mÉÉhQÒû uÉhÉï or μÉåiÉ, MühQÒû, xÉÑÎmiÉ, aÉÑÂiuÉ Grows slowly Associated with pain, numbness, itching.

mÉÉhQÒû uÉhÉï UÉåqÉ, iuÉcÉÉ vÉÏiÉ ÎxlÉakÉ qÉ×SÒ ÎxjÉU, xsɤhÉ EwhÉÉæcNûÉ MüÌPûhÉ ÌlÉSì, uÉqÉlÉ, AÎalÉqÉÉlkrÉ After pressing the pit will not reappear in the night condition get aggravated. ÌlÉzÉuÉsÉÈ

aÉÑÂ

ÎxjÉU mÉÉhQÒû uÉhÉï, pÉÉåeÉlÉÉÌS mÉëÌiÉAÂÍcÉ

AÎalÉqÉÉl±, mÉëxÉåMü, ÌlÉSìÉÍkÉMü, uÉqÉlÉ mÉëuÉëÑ̨É

Takes longer time to appear and cure After pressing the pit will not reappear In the night condition gets aggravated.

Dwidoshaja shotha:

According to Vagbhata:

The causes of two doshas will have their respective symptoms appear in

simultaneously.

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Table No. 2.7 Dvidoshaja

cÉUMü xÉÑ´ÉÑiÉ uÉÉapÉOû95 ̲SÉåwÉeÉ vÉÉåjÉ ---

---

Symptoms are not clearly mentioned but two SÉåwÉ symptoms represents present state.28

SANNIPATAJA SHOTHA

According to Charaka:

The shotha due to the combination of two doshas may be diagnosed by on the

basis of combined etiology, signs and symptoms. Similarly Sannipataja type of shotha

can also be diagnosed from the combinations of etiological factor .

According to Sushruta:

It is having symptoms of all the three doshas which will associates with colour

(Varna & Vedana) pain.

Table No. 2.8 xÉ̳ÉmÉÉiÉeÉ vÉÉåjÉÈ

cÉUMü96 xÉÑ´ÉÑiÉ97 uÉÉapÉOû xÉ̳ÉmÉÉiÉeÉ All symptoms represents after

the combination of all three SÉåwÉ s.

All symptoms represents after the combination of all three SÉåwÉ s along with discoloration and pain.

---

RAKTAJA SHOTHA

According to Sushruta:

All the symptoms will be similar to the pittaja shotha and which represent the

raktaja shotha but will be more blackish in colour31.

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Table No. 2.9 U£üeÉ vÉÉåjÉÈ

cÉUMü xÉÑ´ÉÑiÉ98 uÉÉapÉOû U£üeÉ

---

All symptoms like ÌmɨÉeÉ but it will be more blackish.31

---

ABHIGHATAJA SHOTHA

According to Vagbhata:

Abhighataja is that, which is caused by cutting, splitting, hitting etc. by sharp and

other kinds of weapons, by snow and cold breeze, touch by the juice of Bhallatak, hairs

of Kapikacchu, and sharp spikes (of grains etc.) shotha spreads from place to place is

very hot to touch, resembles blood in colour and usually having symptoms of pitta32.

Table No. 2.10 AípɱÉiÉeÉ vÉÉåjÉÈ

cÉUMü xÉÑ´ÉÑiÉ99 uÉÉapÉOû100 AípɱÉiÉeÉ

--- ÌmɨÉ, U£üeÉurÉ aÉÉåjÉsɤÉhÉ

Swelling spreads from place to place symptoms like ÌmɨÉeÉ present.

VISHAJA SHOTHA

According to Vagbhata:

Vishaja (caused by poison) is that produced by crawling or urinating over the

body, injuries by the tusks, teeth or claws of poisonous animals or even by the contact of

the excreta, urine, semen or cloths of even non poisonous animals, touch of poisonous

trees, wind (gas, smoke, fumes of poisonous nature) and rubbing of artificial poisons etc.

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such a shotha is sof, movable, drooping down, quick to manifest and causing burning

sensation and pain.

Table No. 2.11 ÌuÉwÉeÉ vÉÉåjÉÈ

cÉUMü xÉÑ´ÉÑiÉ uÉÉapÉOû101 ÌuÉwÉeÉ

--- ---

Quick to manifest qÉ×SÒ cÉsÉ SÉWû vÉÔsÉ AkÉÉåaÉqÉlÉzÉÏsÉ (AuÉsÉqoÉÏ)

According to Madhava Nidana – Vishesha lakshana

Vataja – Vishamam pachyata, No particular time for ripening.

Pittaja – Achira – ripens quickly

Kapahja – chiram – slow process of ripening.

Three stages of Vranashadha (inflammation)

Amashotha lakshana – Mando shmata, Alpa shotha, katinyata, Twak savarnata, Manda

vedana.

Pachyamanashotha lakshana – There is a violent pain as that of pricking by needle,

Burning or cauterizing, Pricking by knife, scorpionor, Ant-bite like the patient will be

restless irrespective of position, the tumor gets elevated like blown leather bag, the skin

becomes pale, there will be fever, heat, thirst & loss of appetite.

Pakwa shotha lakshana – In pakwa condition pain relaxes, witish skin, Diminished

swelling, wrinkles appear on the skin, occasional itching.

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Sushruta and Madhava are of the opinion that in shotha there is involvement of all

the three doshas. Ruja is because of vata, Paka is because of pitta and puya is because of

kapha.

SADHYASADHYATA102

Before going to start the chikista of a particular disease, one should know about

the sadhyasadhyata of a disease, i.e. whether it is easily curable, with efforts or incurable

etc should be known. According to prabhava, the diseases are classified as sadhya and

asadhya. Sadhya is subdivided a sukha sadhya and krichra sadhya where as asadhya is

subdivided as yapya and pratyakhya.

If the rogi is krisha or Durbala or if associated with upadravas, when it moves to

the marma sthana, ruja yukta and associated with srava and sarvangashotha is considered

to be asadhya. Where as in aheenamamsa, ekadoshaja, nava, balavan vyakti shotha is

sukha saadhya.

UPADRAVA

Chardi, trishna aruchi,swasa, jwara, atisara,dourbalya, pipasa, hikka, kasa are the

updravas of shotha.

CHIKITSA SOOTRA103

Depending on bala, dosha and kaala, one has to see the nidana, dosha, rutu and

viparita chikitsa has to be done.

CHIKITSA104

Samanya chikitsa

1. Amavastha - langhana, pachana

2. Prakupitavastha – Vamana, Virechanadi vishodhana

3. Shotha in shira pradesha- shiro virechana

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4. Shotha in urdhwa bhaga – vamana

5. Shotha in Adhava pradesha – virechana

6. Shotha because of snehapana – Rukshakarma

7. Malavibandhata in vataja shotha – Niruha basti.

Oushadhis used in Shotha

1. Gandiradyarishta

2. Astashataarista

3. Punarnavadyarishta

4. Phalatrikaadyarishta

5. Kshragutika

6. Kamsaharitaki

7. Chitrakaghrita.

8. Dashamoola kwatha

9. Abhayadhi kwatha

10. Shothari choornam

PATHYAPATHYA105

Pathya

Kulatha yusha, Trikatu, Yavakshara choorna, Mudga, Jangala pashu pakshi

mamsa, Koorma, Shiki, Shallka mamsa rasa, Sauvarchala, Grinjana, Patola, Vayasi,

Moolaka, Nimba, one year old Yava and Purana Shaali.

Apathya

Gramya, Jaleeya, Anupa mamsa, Lavana, Shushka, Navanna, Gouda (Guda

Padartha), Pishtanna, Dadhi, Tila, Madya, Amladravya vallura, Samashana,

Guru,Asatmya, Vidahi anna, Divaswapna and Maithuna.

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List of Single Drugs used as Shothahara.

Bilwa Agnimantha Jayanti

Shyonaka Pathala Punarnava

Kashmarya Prashniparni Harenuka

Shalaparni Brahati Apamarga

Kantakari Gokshura Twak

Shunti Patha Ela

Rasna Yashti madhu Tejapatra

Patola Rakta chandana Nagakeshra

Daru haridra Chitraka Indrayava

Nirgundi Apamarga Pippali

Bringaraja Eranda Danti

Priyangu Kushta Maricha

Vacha Chavya Ajamoda

Haridra Moolaka Katphala

Karkata shringi Katphala Pamakashata

Hingu Manjistha Kokilaksha

Nimba Guggulu Grinjanaka

Guduchi Kapitha

Jeeraka Paribhadra

Kulaththa Ashwatha

Amra Balataka

Haritaki Amalaki

Bibitaki Dathoor

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REVIEW OF INFLAMMATION

DEFINITION:

Inflammation is defined as the local response of living mammalian tissues to

injury due to any agent. It is a body defense reaction in order to eliminate or limit the

spread of injurious agent as well as to remove the consequent necrosed cells and

tissues.

HISTORICAL BACKGROUND

The features of inflammation were described in an Egyptian paper around

3000 BC. celsus, a Roman writer of the first century AD listed the four cardinal signs

of inflammation, they were rubor (redness) tumor (swelling), calor (heat) and dolor

(pain). These signs are more prominent in acute inflammation than in chronic

inflammation. Later Virechow added the fifth sign of functiolaesa (loss of function).

Inflammation is not a disease but a non-specific response that has a saluton

effect on its host, this obvious fact was noticed by the Scottish surgeon John Hunter in

1793.

Julius Cohnheim (1839-1884) who provided one of the first and best

microscopic description of inflammation and observed inflamed blood vessels in thin

and transparent membranes such as in the mesentery and tongue of frog. Noting the

initial vasolidation and changes in blood flow, the subsequent oedema caused by

increased vascular permeability and the characteristic leukocyte emigration.

Elie Metchnikoff, a Russian biologist in 1882 discovered the process of

phagocytosis by observing the ingestion of rose thorns by amebocytes of starfish

larvae and of bacteria by mammalian leukocytes and concluded that the purpose of

inflammation was to bring phagocytic cells to the injured area to engulf invading

bacteria. Metchnikoff contradicted the prevailing theory, that the purpose of

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inflammation (humoral theory of immunity) was to bring in factors from the serum to

neutrilize the infectious agents. It became clear that both cells (phagocytes) and serum

factors (antibodies) were critical for defense against micro-organisms, this

strengthened by the discovery of the antitoxins by Behring and Kitasato (1890)

On the basis of simple experimental studies of inflammatory response on skin.

Sir Thomas Lewis established the concept that chemical substances such as histamine

locally induced by injury, mediate the vascular changes of inflammation, this

fundamental concept underlies the important discoveries of chemical mediators of

inflammation and the use of anti-inflammatory agents.

CAUSES OF INFLAMMATION

The agents causing inflammation are

1. Physical agents like heat, cold radiation, mechanical trauma.

2. Chemical agents like organic and inorganic poisons

3. Infective agents like bacteria, viruses and their toxins

4. Immunological agents like cell mediated and antigen antibody reactions.

Thus, Inflammation is distinct from infection- the former being a protective

response by the body while the latter is invasion into the body by harmful microbe &

their resultant ill effects by toxins.

Inflammation involves two basic proceses

• Inflammatory response

• Healing

Though both these processes generally have protective role against injurious

agents. Inflammation and healing may cause considerable harm to the body as

well. Ex: Anaphylaxis to bites by insects or reptiles, drugs, toxins, atherosclerosis

chronic RA, fibrous bands & adhesions in intestinal obstruction.

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SIGNS AND SYMPTOMS

The Roman writer Celsus described four cardinal signs of inflammation as

(a) Rubor (Redness): An acutely inflamed tissue appears red due to dilatation of

small blood vessels within the damaged area.

E.g., Skin affected by sunburn, cellulites by bacterial infection etc.

(b) Calor (Heat): Increase in temperature is seen only in peripheral parts of the

body such as skin. It is due to increased blood flow (hyperaemia) through the

region resulting in vascular dilatation and delivery of warm blood to the area.

E.g., Systemic fever.

(c) Tumor (Swelling): Swelling results from oedema, the accumulation of fluid in

the extra vascular space as part of the fluid exudates and to a much lesser

extent, from the physical mass of the inflammatory cells migrating into the

area.

(d) Dolor (Pain): Pain is the best-known feature of acute inflammation. It results

partly from stretching and distortion of tissues due to inflammatory oedema

and in particular from pus under pressure in an abscess cavity. Chemical

mediators like bradykinin, prostglandins and serotonin are known to induce

pain.

(e) Loss of function (Functio laesa): Movement of an inflamed area is consciously

and reflexly inhibited by pain, while severe swelling may physically

immobilize the tissues.

CLASSIFICATION OF INFLAMMATION

Inflammation may be classified on the basis of various factors.

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I) Based on duration & severity

Depending upon the defense capacity of the host & duration of response,

inflammation can be classified as acute & chronic.

Acute inflammation – It is of short duration & represents the early body reaction &

is usually followed by repair.

The main features of acute inflammation are –

1) Accumulation of fluid & plasma at the affected site.

2) Intravascular activation of platelets.

3) Polymorphonuclear neutrophils as inflammatory cells.

Chronic Inflammation – It is of longer duration & occurs either after the causative

agents of acute inflammation persists for a long time or the stimulus such that it

induces chronic inflammation from the beginning.

The characteristics features of chronic inflammation is presence of chronic

inflammatory cells such as lymphocytes, plasma cells & macrophages.

II) Based on the Nature of exudates

• Serous

• Fibrous

• Haemorrhage

• Purulent

• Catarrhal

III) Based on causative factors

• Tubular

• Syphilitic

• Staphylococci

• Foreign body reaction

• Allergic

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I. ACUTE INFLAMMATION:

a) CATARRHAL ACUTE INFLAMMATION:

This is confined to mucous membrane, the mucous cells of the lining and of

the mucous glands secrete large quantities of mucin, there is molecular desquamation

of the surface lining, not so pronounced as to appear as ulceration. The discharge on

the surface or in the lumen consists of mucous plasma, leucocytes and desquamated

epithelial cells, it is mucoid in the early stages and becomes mucopurulent later.

Acute catarrhal inflammation is mildest form of inflammation, but in some organs it

can progress to termination and can become chronic. E.g. Rhinitis of common cold,

catarrhal bronchitis.

b) FIBRINOUS OR SEROFIBRINOUS INFLAMMATION:

This is seen in the serous membranes, the pericardium, pleura, peritoneum etc.

It consists of plenty of fibrin in the exudates derived from the exudate plasma,

irrespective of the nature of the irritant, they react in a stereotyped manner.

Neutrophils and macrophages are seen in the fibrinous network.

c) SUPPURATIVE OR PURULENT INFLAMMATION:

This type is characterized by the formation of pus. In solid tissues and organs

suppurative inflammation causes Abscesses, in contrast to the circumscribed affection

in abscess formation the process may become diffuse and spreading. Diffuse lesions

in the connective tissue are described as “Phlegmonous Inflammation or Cellulites”.

d) ACUTE HAEMORRHAGIC INFLAMMATION:

In certain cases, bacterial toxins produce intense injury to the capillary wall

and allow large number of Red Blood Corpuscles to escape, making the exudates

haemorrhagic. E.g. In Influenza Pneumonia, Acute Glomerulonephritis etc.

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e) PSEUDO MEMBRANOUS INFLAMMATION:

This form of inflammatory reaction is characterized by the formation of a

membrane usually made up of precipitated fibrin, necrotic epithelium and

inflammatory white cells. The reaction is encountered only on mucosal surfaces

commonly in the Pharynx, Larynx, Respiratory passage etc. The membrane formation

results from an acute inflammation response to a powerful necrotizing toxin, out

pouring of exudates traps the necrotic and cellular debris producing a dirty gray-

white, rubbery membrane on the eroded surfaces. E.g. In Diphtheria.

f) ALLERGIC INFLAMMATION:

In this, Inflammation is primarily and exclusively by antigen-antibody

reactions. The injury in this is due to the occurrence of antigen-antibody union on

walls of the tissue cells, hypersensitivity has much greater significance. The vascular

changes are associated with a cellular exudates consisting of neutrophils, eosinophils,

plasma cells and macrophages. Eosinophils may be spectacular components, tendency

to necrosis and tissue decay due to accelerated reaction and increase in the Phagocytic

power of the Leucocytes with increase of eosinophils are distinct features in allergic

inflammation.

2. CHRONIC INFLAMMATION

The acute inflammatory response is unable to remove or neutralize an

injurious agent; the response is modified to chronic. It is not usual for a chronic

response to last many months but years. As the inflammatory process continues, fluid

exudates diminishes and cellular response assumes dominance, the chronic response

is dominated by a massive build up of cells in the affected tissue. These cells are

primarily macrophages and lymphocytes. In chronic inflammation the agent and the

host are just capable of resisting each other. The agents involved are of low inevitable

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ability. They are unable to penetrate deeply in to or spread throughout the body of the

host. Such agents may be bacteria, fungi, larger parasites. Foreign bodies which are

insoluble in body’s fluid can also elicit a chronic inflammatory response.

Regardless of the specific nature of the inciting agent, its presence in the tissue

promotes a long term conflict with the phagocytic cells of the host; heavy infiltration

by the inflammatory cells progressively interferes with normal function. When the

process continues over a month and years, the function detoriates as tissue is

destroyed, accumulating inflammatory cells replace functional tissues and scarring

develops. This deterioration ultimately leads to somatic death.

TYPES OF CHRONIC INFLAMMATIONS

Following Four types are included in Chronic Inflammation:

1) Chronic Diffused Inflammation

2) Chronic Suppurative Inflammation

3) Chronic Granulomatous Inflammation and

4) Chronic Fibrinoid Inflammation.

1) CHRONIC DIFFUSED INFLAMMATION:

Exudates, which may be diffused or focal shows lymphocytes, plasma cells

and macrophages, under certain stimuli macrophages develop into epitheloid cells and

multinucleated giant cells. Fibroblasts are present, in older lesions fibrosis

conspicuous. E.g. Chronic Ulcer.

2) CHRONIC SUPPURATIVE INFLAMMATION:

It is a non-specific inflammatory cell infilteration, in which infiltration by

polymorphs and abscess formation. E.g. Actinomycosis

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3) CHRONIC GRANULOMATOUS INFLAMMATION:

It is characterized by the formation of Granulomas, a tiny lesion composed of

epithelial cells and lymphoid cells at the periphery, also granulomas may have giant

cells, necrosis and fibrosis. It is seen in specific infective granulomas as in

Tuberculosis, syphilis. Leprosy etc.

4) CHRONIC FIBRINOID INFLAMMATION:

It is a degenerative phenomenon like rheumatoid arthritis, reheumatic fever etc.

TABLE NO 2.12 Differences between acute inflammation & chronic

inflammation

Acute inflammation Chronic Inflammation

1.Duration: Usually for days or weeks 1. Duration: For months or Years

2. Cardinal Signs: Present 2. Cardinal Signs: Doubtful or not

perceptible

3.Vascular Changes: Present 3.Vascular Changes: Not Marked

4. Exudation of Plasma: Present 4. Exudation of Plasma: Doubtful or

Absent

5. Cellular Exudates:

Neutrophils initially lates Macrophages and

Fibroblasts Stage of repair Lymphocytes

are few.

5.Cellular Exudates:

Histocytes Plasma cells lymphocytes

Fibroblasts are present Neutrophils

absent or very less in numbers.

7. GENERAL MECHANISM OF INFLAMMATION

The starting point of inflammation is the cell damage, living or inert, the cells

which do not damage are not capable of producing inflammation. However once the

damage has occurred the reaction takes place inevitably and proceeds through a

definite series of events to its ultimate end, i.e. repair of damage and restoration of

function.

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GENERAL MECHANISM OF INFLAMMATION

• Vascular phenomenon changes

Vasodilation

Active hyperemia

Capillary dilation

Static of blood

Sludging of red cells in the capillaries

Pavementation of leukocytes

Exudation of fluid and out pouring of polymorphs

• Cellular response

Local

Exudation

Fluid of exudation

Cells of the exudation

General response

Fever degeneration

Leukocytosis

• Repair of tissues

Degenerative

Albuminous degeneration

a. Repuls degeneration

b. Healing cloudy swelling

c. Regeneration

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Fatty degeneration

a. Suppuration

b. Abusers

c. Boil

d. Carbuncle

e. Cellulites

Proliferative

Phagocytes

a. Attachment

b. Engulfment

(i) Azophil

(ii) Special groused

c. Killing and degeneration

(i) Oxygen dependent mechanism

(ii) Oxygen independent mechanism

Cells included in the inflammatory exudates are :

• Neutrophil

• Eosinophils

• Mast cells

• Lymphocytes

• Plasma cells

• Macrophages

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MECHANISM OF INFLAMMATION -

Management of inflammation and action of non-steroidal anti-inflammatory drug.

Irrespective of the nature of causative factors or the type of inflammation, the

tissue reaction in first few hours is stereotyped and similar. Its pathology can be

understood in the fallowing steps.

1.Vascular phenomenon

2.Cellular phenomenon

3.Repair

1.Vascular phenomenon:

Following changes will occur in vascular phenomenon one by one

i. Vasodilatation: Proceeded by transient vasoconstriction

ii. Active hyperemia

iii. Capillary dilatation

iv. Stasis of Blood

v. Sludging of red cells in the capillaries.

vi. Pavementation of leukocytes.

vii. Exudation of fluid and out pouring of polymorphs.

There are number of cells present in the inflammatory exudates which perform

various functions. Those are

a. Neutrophils

b. Eosinophils

c. Mast cells

d. Lymphocytes

e. Plasma cells

f. Macrophages

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A brief description and the role is as follows.

a) Neutrophils: Neutrophils or Polymorphs are the cells along with Basophils and

Eosinophils are known as granulocytes, due to the presence of granules in the

cytoplasm, contains substances like proteases,myloperoxidase and alkaline

phosphates. Neutrophils are actively motile, get collected arround blood

vessels and passes through the tissue by active amoeboid movements, there

from the first line of defense in bacterial infections.

b) Eosinophils: These are larger than the Neutrophils and constitute 2-4% of the

total blood leucocytes. They appear only at the sites of inflammatory exudates

of diseases of immunological origin. They remain in the circulation for a short

peroid and rapidly attracted in the tiisues by the raised concentration of

released histamine. Eosinophils are phagocytic in nature. These may share

many structural and functional similarities with neutrophils, like their

production in the bone marrow, locomotion, lobed nucleus and presence of

granules in the cytoplasm. Granules of eosinophils are rich in

myeloperoxidase than neutrophils and lack lysozyme. High level of steroid

harmone (eosinopenia) leads to fall in number, and even disappear from the

blood. These may be increased in certain conditions like Allergy, Parasitic

infestations, skin diseases and certain malignant lymphomas.

c) Mast cells: These cells contain coarse basophilic granules in the cytoplasm

and a polymorphous nucleus, These granules are laden with heparin and

histamine. The functions of mast cells in normal Human being is not vivid.

They are believed to produce the acid.

d) Plasma cells: These are larger than the lymphocytes with more abundant

cytoplasm and an eccentric nucleus. These cells are normally not seen in

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peripheral blood. They develop from lymphocytes and are rich in RNA and

Gama-globulin in their cytoplasm. There is an inter relationship between

Plasmocytosis and Hyperglobulinaemia. These cells are most active in

antibody synthesis. The number will increase when prolonged infection with

immunological responses. e.g. Syphilis, Rheumatoid Arthritis, Tuberculosis,

Hypersensitivity states and multiple myeloma.

e) Macrophages: These are large mono-nucleated cells play an important role in

the stages of Acute and Chronic Inflammations. It is believed that many

lymphocytes derived from the blood are converted in to microphages at the

site of inflammation, by increase in cytoplasm and enlargement of the nucleus

and are derived from Kuffer cells of the liver and histocytes. They form the

scavenger cells of inflammation, combine to form giant cells and need

phagocytic action. The giant cells are mainly of :

i. Tumour Giant Cells

a. Anaplastic Cancer Giant Cells

b. Reed-Sternberg Giant Cells and

c. Giant Cells of Tumour

ii. Foreign Body Giant Cells.

i. Tumour Giant Cells: It is of fallowing types

a. Anaplastic Cancer Giant Cells:

These are larger and have numerous nuclei which are hyper chromatic and

vary in size. These giant cells are not derived from macrophages but are formed from

dividing nuclei of the neoplastic cells.

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b. Reed-Sternberg Giant Cells:

These are malignant tumour giant cells , which are binucleate and are seen in

various histologic types of Hodgkin's lymphomas.

c. Giant Cells of Tumour:

These cells are usually found in the bones, uniform distribution and

osteoclastic giant cells spread in the stroma.

ii. Foreign Body Giant Cells:-

These contain numerous nuclei, which are uniform in size and shape and

resemble the nuclei of macrophages, these nuclei are scattered throughout the

cytoplasm, these are usually seen in the chronic infective granulomas.

2.CELLULAR RESPONSE:

Cellular response can be explained in to a) Local response and b) General

response. The local response starts with the pavementing and emigration of

leukocytes before the cells of the damaged tissue release some chemicals that bring

about all the changes. The Vasodilation and increased permeability is due to the

substances like "leukotoxin" and "histamines" are produced by the damaged tissue

cells.

These stimuli activate both Hematogenic and Histogenic cells, which carry out

various functions like vascular phenomenon, pavementation and emigration of

leukocytes and various other cellular responses.

Following a local injury, there is a transient constriction in the vessels that

cause local Ischemia. This mommentary constriction is followed by an active phase of

hyperemia with dilation of vessels, this dilation chiefly occurs in arteries and venules

and at last in the capillary bed. The active hyperemia lasts for a few hours. The

capillaries get changed and become prominent.

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The blood vessels keep on dilating and the active hyperemia is fallowed by the

stagnation of blood, which is termed as stasis and the clotting takes place in the

vessels. The blood supply to the tissue is lost and necrosis sets in the vasodilation that

follows the transient vasoconstriction (due to neural reflex) It is recognized that a

sensory fibre has a vasodilator branch to an arteriole. When there is an injury, there is

a reflex vasoconstriction and thus vasodilation sets in.

The vasodilation occurs under the influence of chemical mediators also, it was

postulated by Lewis (1927) that "H" like substance cause vasodilation. Further

Menklin postulated about "Leukotoxin". In addition, it increases the vascular

permeability and responsible for the emigration of leukocytes, the slowing of blood

flow in the vessels may be attributed to swelling of the endothelial lining of the blood

vessels, vasodilatation that decreases the pressure. Loss of blood fluid in interstitial

spaces makes the blood viscous. There is sludging of red cells. The red cells become

sticky and adhere to one another in masses and to the walls of the vessels.

In this slower blood stream, rearrangement of the corpuscles takes place, under

normal condition, the red and white cells flow intermingled in the central part of the

vessels forming an axial stream, which is separated from the wall by a clear plasmatic

zone free from cells. When there is some degree of injury, the leukocytes fall out of

the axial stream and come to occupy the plasmatic zone adhere to the vessel wall and

seem to drag themselves along with difficulty. In this way, the inner wall of the

capillary becomes paved by a broken line of leukocytes without the admixture of a

single red blood cell. This arrangement is called pavementing of leukocytes.

Normally the endothelial cells of the blood vessels and blood cells repel one

another due to change in the electrical potential, where these carry negative charges

with them, hence the repulsion. The endothelium becomes positvely charged and the

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leukocytes are the first of the cellular elements to be attracted to and adhere to the

lining of the vessel.

The endothelial cells also become enlarged, proliferated and thus assume

round shape. The inter-endothelial space widens and through these spaces leukocytes

emigrate.

A) EXUDATION:

After dilation of blood vessels, the solid and fluid contents of plasma as well

as of the blood cells pass through the vessel walls and constitute within the tissues.

Thus, the fluid is rich in protein contents and the cells constitute the exudates.

B) FLUID OF THE EXUDATE:

Normally the walls of the blood vessels are permeable to the fluid, some ionic

salts and the molecules with molecular weight less than 10,000 Daltons, large part of

the fluid get reabsorbed and the remaining is carried by lymph channels.

But during inflammation, this exudate fluid, which originates from plasma

differs from it in several aspects. Its solid contents are almost double than the contents

of the lymph. Its specific gravity is 1.020. The main reason is that serum albumin and

serum globulin is present in exudate. The fluid molecules come out of vessels due to

increased permeability of vessels.

Besides this protein, the exudate contains various extractions like Urea, fibrin

forming elements, mucin ferments and immune bodies, oxidases, lipases and trysin.

All type of immune bodies may be found including cytolysin, haemolysin,

bacteriolysin, agglutinins, opsonins and complement fixing bodies. The formats and

the immune substances are distinctly higher in oedema than oedema produced due to

other causes.

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FUNCTION OF FLUIDS OF EXUDATE :

1. It dilutes the soluble poisons and irritates, thereby reduces their direct effect.

2. It provides over runs of escape for the metabolites which are formed in excess.

3. It maintains normal hydrogen concentration.

The protolytic enzymes serve to complete the solution of the tissues which

have been injured or killed, thus aid in their removal. Exudate is rich in fibrin forming

proteins. The environment in which it is present favours fibrin formation, this serves

as the limits of extent of the inflammatory process. The fibrin mesh in the lymphatics

serve as a filter and with solid materials especially bacteria, if it is not dissolving by

protolytic enzymes it provides a frame work on which connective tissue grows and

healing takes place.

C) CELLS OF THE EXUDATES:

After pavementing the leukocytes emigrate in extra vascular spaces, as they

emerge from the outer margin of endothelium, a new basement membrane forms

between them and the endothelium disappears permitting release of the leukocytes in

to the extra vascular space without leaving any defect behind them, under the

influence of various chemical mediators, this phenomenon is known as "Chemotaxis".

D) PHAGOCYTES:

Phagocytes can be resolved in to three distinct ways

1. Attachment of the Particle to the surface of the phagocyte.

2. Engulfment.

3. Killing and degeneration of the ingested microbe or particle.

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1. ATTACHMENT OF THE PARTICLE TO THE SURFACE OF THE

PHAGOCYTE:

These cells are recognized and attracted to bacteria by chemotactic factors

released by bacterial products as well as by tissue proteins, in order to establish a

bond between bacteria and the cell membrane of phagocytic cells, the micro

organisms get coated with opsonins which are naturally occurring factors in the

serum.

The main opsonin present in the serum IgG opsonin, is the Fe fragment of

immunoglobulin G, antibody in the serum that coats the bacteria. C3b opsonin is the

fragment of completement, which is generated by activation of completement

pathway.

Lactins are carbohydrate-bonding proteins in the plasma, which bind to

bacterial cell wall. Receptors mediated attachment of opsonized bacteria has been the

recognization step of Phagocytosis.

2. ENGULFMENT:

Leukocytes are able to respond to opsonins for that they display leukocyte

binding sites, once an opsonin coated particle is bound to the surface receptors of the

phagocyte, the particle is readily engulfed. Binding of a particle to the phagocytic

membrane elicits the engulfment, the phagocytic membrane flows around the particle

to enclose it in a cytoplasmic phagosome. Granular appearing lysosomes that contain

destructive agents then merge with the phagosome membrane, thereby bringing their

contents in to contact with the particle. As lysosome merge with the phagosomes their

number within the phagocyte are reduced and the phagocyte is degenerated. If the

particle is too large to be easily engulfed i.e. a multicellular parasite. There may be

regurgitation of the granule contents in to the tissue spaces. The leukocytes attempting

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to engulf this large surface experiences frustrated phagocytosis and releases toxic and

degradative substances that damage the basement membrane and the surrounding cells

and the matrix.

The neutrophil cytoplasm contains two types of granules Azusophil and

Specific granules. Lysosomes contain acid hydrolases, neutral proteases, cationic

proteins, lysozyme.

i) AZUSOPHIL:

These lysosomes contain acid hydrolases, neutral proteases, cationic proteins,

lysozyme.

ii) SPECIFIC GRANULES:

Which contain lysozyme and lectoferiin but no hydrolases or peroxides.

Macrophages also contain azusophil granule. The process of degranulation pour in to

the phagosome powerful enzymes which kill the bacteria by different mechanisms.

3. KILLING AND DEGENARATION:

The micro-organisms after being killed by antibacterial substances are

degraded by hydrolytic enzymes, their mechanism fails to kill and degrade some

bacteria.These are of mainly two types, Oxygen dependent and Oxygen Independent.

1. Oxygen dependent:

It is an important mechanism of microbicidal killing by the production of

reactive oxygen metabolites (O2 H2O2, OH, HOCL, HOL, HOBr) a phase of increased

oxygen consumption by activated phagocytic leukocytes in presence of NADPH

oxidase.The NADPH oxidase which is present in the cell membrane of phagosome

reduces oxygen to superoxide ion (O2).

2O2 NADPH 2O2 (superoxide anion)

2O2 + 2H─ H2O2

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Suproxide is subsequently converted in to Hydrogen peroxide (H2O2) has

bactericidal properties, this bactericidal activity is carried out either enzyme

myeloperoxidase present in the granules of neutrophils and monocytes or the enzyme

myeloperoxidse acts on Hydrogen peroxide in the presence of halides (Chlorides,

Iodide, Bromides) to form hypophalous acid (HOCl ). Which is more potent

antibacterial agent than hydrogen peroxide.

Reactive oxygen metabolites are useful in eliminating microbial organisms

that grow within phagocytes.

2. OXYGEN INDEPENDENT:

This mechanism involves the release of substances that damage bacterial cell

walls, disrupt bacterial replication and produce a low pH within the phagosomes

resulting from accelerated glycolysis, Which may be directly toxic and may indirectly

aid the function of other enzymes.

b) GENERAL RESPONSE:

The general celleular respons may be Fever and Leukocytosis.

i. Fever:

Fever is one of the most prominent systemic manifestation, particularly in

inflammation associated with spread of organisms into the blood stream. The patient

may have high fever charecterised by dramatic swings in the temparatur. The origin of

the fever may be uncertain, although it may be caused by the release of bacterial

endotoxins. In addition interleukin – 1 (IL-), prevously described as endogeneous

pyrogen released from the leukocytes is an important mediator of hyper pyrexia. This

mediator is taken up by lymphatics from the site of imflammation, which is circulated

in blood stream. It is believed that IL-1 initiates fever by inducing the synthesis of

PGE2 in the anterior hypothalamas and stimulating thermoregulatory centres.

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ii. LEUKOCYTOSIS:

Increase in the number of circulating white cell is another charecteristic

significance of acute and chronic inflammation. When the inflammation is deep and

the local symptomatology is either not observes or impossible to demonstrate, then

leukocytosis is of assistance in determining the severity of the infection and the

degree of the resistance offered by the body. This requires not only an absolute count

(i.e. the total number of white cells per mm) but also the relative number of each type

of leukocytes particularly the number of neutrophils. In making the differential count,

the number of each kind of white cells in hundred is counted.

• A high absolute count (T.L.C) with a high neutrophil percentage indicate

severe infection and good body resisitance.

• A high absolute count with a moderate neutrophil percentage indicates a

moderate infection and good body resisitance.

• A low absolute count with high neutrophil percentage indicates severe

infection and weak resisitance of the body.

• All inflammatory states do not evoke neutrophilic leukocytosis. Infectious

mono nucleoses, whooping cough, mumps, rubella and undulent fever

charecteristicaly produce lymphocytosis.

Allergic inflammatory reaction like hay fever, bronchial asthama and parasitic

infection typically elicit eosinophilia. Some infections may cause leukopenia instead,

like infections caused by viruses, rickettsiae, protozoa and salmonelloses.

C. TISSUE CHANGES OR REPAIR:

There are two types of tissue changes

a. Degenerative

b. Proliferative.

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a. DEGENERATIVE:

The two most common degenerations are

1. Albuminous degeneration or cloudy swelling

2. FATTY DEGENERATION

1. Albuminous degeneration or cloudy swelling:

It is closely related to hydrophic or vascular degeneration. Being manifestation

of a disturbance of protein metabolism, is called as Albuminous degeneration. It may

be caused by the bacterial toxins, chemical poison, malnutrition and other

disturbances.

The principle organs showing cloudy swelling are Kidneys, Liver and Heart

muscles. The organ affected is slightly enlarged owing to swelling of the cells of

which it is composed. It is pale as blood vessels being compressed by the swollen

cells. The cut surface has rather cloudy appearance and slightly opaque.

2. FATTY DEGENERATION:

Fatty degeneration or Fatty metamorphosis is a true sickness of cells caused

by some injurious influences. It is best seen in Liver, Kidney and Myocardium. The

fat metabolism is interferred with fat accumulations in the cell. In some cases there is

merely unmarking of fat already present. The causes of fatty degenerations are

• Poisons

• Anoxia

The organs look fatty. The liver and kidneys are pallor and softer than normal.

The heart is soft and flabby. Ultimately the tissue becomes necrosed.

If the irritant is intense, the effect is degenerative destruction. If it is mild, acts

as stimulant and leads to proliferation. At the centre of the inflammatory area the

action of the irritant is severe, degeneration predominates at the periphery and the

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action is mild. The tissue may be stimulated to proliferation. thus this part of the

inflammation is known as repair or healing.

i) SUPPURATION:

If the dead tissue in an inflammed area undergoes softening and liquification is

known as the process of Suppuration, the fluid formed is called the Pus, by this

method the dead material is removed from the body.There are three requisites for

suppuration.

i. Necrosis

ii. Presence of sufficient leukocytes

iii. Digestion of the dead materials by protolytic fermentation.

If any one of these are absent suppuration does not occurs.The digestive

enzymes are produced mainly by the leukocytes to a lesser extent by the necrosed

tissue cells and the infecting bacteria. These are neutralized by anti enzymes present

in the serum. If there is less leukocytes or more serum liquification does not take

place.

ii. ABSCESS:

It is an example of a localized suppuration. The inflammation is limited to the

area and as the irritant is pyogenic, pus is produced. The cells in the centre of the

inflammatory area are killed and liquified by protolytic enzymes. In this way a cavity

is produced which contains pus. The wall of the abscess cavity consists of damaged

but still living tissues. Hence the spread of infection is limited, this limiting zone is

crowded with polymorph nucleus leukocytes and macrophages filled with debris. Pus

cells are continuously dicharged from this, thus the abscess is chronic or if the

infection is dying out, the macrophages will greatly outnumber the polymorphs

further out, the tissue become more and more normal.

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If the infection is continuously active more and more material is added to the

abscess, So that the pressure within the abscess increases. Thus it points in the

direction of less resistance. If the abscess enters the muscle sheath, it may extent

along a considerable distance.

iii. BOIL:

It is an abscess of a Sebaceous gland or a hair follicle caused by the

Staphylococcus aureus, which has penetrated the opening of the duct. There is a

marked fibroblastic proliferation, which with intercellular formation of fibrin, causes

the characteristic indusation. The tension becomes high and causes pain. There may

be a very little liquification of the necrosed tissue, So that the centre of the boil is

composed of a solid "Core" instead of Pus.

iv. CARBUNCLE:

It is the infection spread to the subcutaneous tissue where it causes a more

diffused lesion which discharges on the surface by a series of openings. The pus

becomes inspected and the dead tissue is converted into a mass of fatty debris in

which lime salts may be deposited.

v. CELLULITIS:

When the suppuration spreads through the tissues, the condition is called

cellulitis. The fibrin that forms as a result of proliferation, inflammed part limit the

infection.

3. REGENERATION:

This implies to a complete renewal of the tissue as in liver. The process of

healing if fundamentally the same in all the wounds. It consists of two parts. Removal

of inflammatory material and necrotic debris, which may be more or little.

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Replacement or reconstruction of the original tissue to a greater degree as much as

possible.

The repair involves the invasion and replacement of dying and dead tissue by

immature mesenchyma called Granulation tissue, which is a highly vascular tissue.

On account of its cellularity a granulating surface has a remarkable power of

resistance against bacterial infection. The granulation tissue grows to maturity from

below to up words. When the wound is aseptic the epithelium will grow in from the

edges as a delicate blue pellicles, gradually it becomes thick and opaque.

When the surface is covered by epithelium, the process of devascularization

begins. The new vessels, being no more needed will gradually disappear. The scar that

is red becomes white and bloodless106.

REVIEW OF ANTI-INFLAMMATION

Drugs which can normally be used to almost every type of inflammatory

conditions are known as anti-inflammatory drugs These have two major groups.

1. Steroidal anti-inflammatory drugs in the form of gluco corticoids.

2. Non-Steroid anti-inflammatory drugs (NSAID)

Mode of action of steroidal anti-inflammatory drugs

ACTH and Glucocorticoids prevent the clinical features of inflammation i.e.

local heat, redness pain and swelling. Their action is based on reducing the increased

permeability of capillaries and maintenance of the integrity of the cell membrane

even in the presence of toxins. Stabilization of lysosomes release from the

granulocytes by inhibiting phagocytosis. Also acts on fats phase of inflammation and

inhibits capillary proliferation deposition of collagen cicatrisation. But fibrous tissue

once formed is not dissolve by corticosteroids.

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Hence the anti-inflammatory effect of steroidal therapy is non specific. The

steroid inhibit the phospholipase enzyme which is essential to activate the cell

membrane. This activation release the arachidonic acid, which metabolises to produce

inflammation. But once the chain is initiated it cannot be stopped by the steroidal

therapy, moreover in large doses, it may interface with wound healing.

9. CLASSIFICATION OF ANTI-INFLAMMATION

These are broadly classified into two groups. Narcotic Analgesics or opoid

analgesics and Non-narcotic analgesics or non opoid analgesic or NSAID, non

steroidal anti-inflammatory drugs.

1. NARCOTIC ANALGESICS:

These agents are capable of relieving severe degree of pain but are moderately

or strongly addicting. This group includes opoids which binds to the opoid receptors.

These, further classified in to Natural opium alkaloids ( e.g. Morphin)., Semi-

synthetic opiums (e.g. Diacetyle morphin or acetyle morphin) and Synthetic opoid

(e.g. Pethedine).

2. NON-NARCOTIC ANALGESICS OR NON OPOID ANALGESIC or NSAID:

In this the agents relieve mild to moderate degrees of pain and are considered

as non active. This group includes aspirin analgesic and other analgesics and

antipyretic drugs and these have no affinity for the opoid receptors, but the site of

action is only peripheral and further NSAID is divided in to Potent anti-inflammatory

and good analgesics, Potent anti-inflammatory and good analgesics, Moderate anti-

inflammatory and moderate analgesics and Poor anti-inflammatory and good

analgesics.

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A. POTENT ANTI-INFLAMMATORY AND GOOD ANALGESICS:

i. Salcylates e.g. Aspirin

2. Oxy cum derivatives e.g. Paraoxicam.

B. POTENT ANTI-INFLAMMATORY AND GOOD ANALGESICS:

i. Pyrazolin derivatives e.g. Phenyl butazone.

ii. In dol derivatives e.g. Indomethacin.

3. MODERATE ANTI-INFLAMMATORY AND MODERATE ANALGESICS:

i. Propyonic acid derivatives e.g. Ibuprofen

ii. Anthranlic derivatives e.g. Mefenamic acid.

iii. Aryl acetic derivatives e.g. Diclofenac.

4. POOR ANTI-INFLAMMATORY AND GOOD ANALGESICS:

i. Para amono phenyl derivatives e.g. Paracetamol or acetaminoidene.

ii. Pyrozolon derivatives e. g. Metamezole.

10. MANAGEMENT OF INFLAMMATION AND ACTION OF NON-

STEROIDAL ANTI INFLAMMATORY DRUGS (NSAID)

As stated earlier, the activation of cell membrane releases arachidonic acid, it

is metabolized by cyclo-oxygenase pathway and produce prostaglandins (PGs).These

include PGG2, PGH2, PGl2, PHE2 and PGE2 and cause vasodilatation and potentiate

oedema. Some of these are supported to inhibit platelet aggregation.

These further sensitize the chemical receptors of the afferent pain endings to

other chemical mediators like bradykinin and histamine. Aspirin and asperin like

NSAID have been shown to inhibit release or synthesis of PG5 and thus produce

beneficial anti-inflammatory condition where PGs are synthesized locally. It is unable

to produce any analgesic effect where the sensory nerves are directly stimulated.

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Some of the NSAID produce anti-inflammatory effect indirectly,like

indomethacin. It inhibits phosphodiesterase and thus increases the intracellular

concentration of cyclic ATP, Cyclic ATP has been shown to stabilize membrane

including lysosomal membrane in polymorphonuclear leukocytes. This prevent the

release of enzymes important in the inflammatory responses. Some drugs may inhibit

the activation of T-lymphocytes which release lymphokinase, which plays an

important role in mediating inflammation107.

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Methodology

METHODOLOGY

Source of drug collection:

The genuine quality of setem bark of devadaru (cedrus devadaru) were

purchased from Alva pharmacy, Moodbidri, Dakshina kannada district. Botanist and

other experts verified the stem bark and its identification confirmed.

Preparation of drug:

Drying the stembark of devadaru:

The stembarks were dried completely under shade to obtain dry barks and also

to minimize the loss of volatile oil.

Powdering:

After proper drying the stembarks were subjected to powdering in pulvarizer

under mesh to get coarse powder and stored in air tight container.

Preparation of extracts:

Extraction of both Aqueous and alcohol extraction of devadaru was done in

Dravya guna department. PG cum Research center DGMAMC Gadag.

Preparation of alcohol extract: Drug- coarse powder of stem bark of devadaru108

We followed the continuous hot percolation process, Drug to extract is packed

in a cylinder made up of filter paper called as Thimble” and is placed in body of

sauxhlet extractor. The solvent is placed in flask apparatus is fitted. When the solvent

is boiling on heating the flask it gets converted to vapour. These vapours enter into the

condensor through the side tube and get condensed into hot liquid, which flak on the

column of the drugs. when extractor gets filled with solvent level of the siphon tube

also raises up to its top solvent containing active constituents of drug in siphon tube,

siphons over and run into the flask, thus emptying the body of the extractor. This

alteration filling and emptying the body of extraction goes on continuously. This

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Methodology

process of filling and empting of extractor is repeated until the drug is exhausted,

normally process is repeated for 15 min for complete exhaustion of drug. Extraction

was done in three batches of these, the extraction process was carried out for about 18

hours to each batch. After the extraction the solvents were distilled off to obtain semi

solid extract & concentrated on magnetic stirrer the weights of each batch of extract

were recorded.

After the effective solvent were concentrated at room temperature in reduced

pressure using evaporator and extraction obtained was weighed its percentage was

calculated. The colour and consistency of extract was noted.

Thus obtained extract was subjected to preliminary phyto chemical

investigation and pharmacological screening for anti inflammatory activity by

carrageenan induced paw oedema method.

Preparation of Aqueous extract109

We followed the cold maceration method. One kg of coarse powder of

devadaru bark soaked in 5 ltr of chloroformed water (to prevent fungal growth) in

closed container for 24 hours, the mixture stirred continuously during first 6 hours and

allowed to stand for next 18 hours, Then the water was filtered completely to a tarred

flat bottomed dish and evaporated to dryness on a water bath. Dry for 6 hours cool in

a dissector for 30 minute. The solid extract thus obtained was weighted & stored in

the glass bottle sealed and kept in refrigerator.

Thus obtained extract was subjected to preliminary phytochemical

investigation & pharmacological screening for Anti inflammatory activity by

carrageenan induced paw oedema method.

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Methodology

Preliminary Phytochemical investigations of extracts110

Qualitative chemical tests were conducted for alcoholic and aqueous extracts

of Devadaru (cedrus deodara) to identify the various phyto constituents. The various

tests and reagent used are given below and observation are recorded.

Material:

Drug: Aqueous & Alcoholic Extractive sample of Devadaru (cedus deodaru)

Equipments: Test tube, holder, stand, spirit lamp, pipette, glass rods, beakere 50 ml

to 250 ml, conical flask, water bath.

Methods

1) Test for sterols:

Salkowaski test A few drops of concentrated sulphuric acid was added to the 5

ml of sample solution (extract) shaken and allowed to stand and observed the lower

layer If it turns to red indicates the presence of sterols.

2) Test for Triterpenoids:

Salkowaski test : A few drops of 10 % concentrated sulphuric acid is added to the 5

ml of sample solution, shaken and allowed to stand (if lower layer turns yellow

indicates the presence of triterpenoids)

3) Test for Glycosides

Keller killiani test: The 5 ml of the solution with few drops of glacial acetic acid in 2

ml of ferric chloride solution and conc H2SO4 is added from the sides of test tube,

then observed for the separation between two layers, if lower layer shows reddish

brown & upper layer turns bluish green indicates the presence of Glycosides.

4) Test for saponins:

Foam test : Sample solution mixed with saponins and shaken, if there is formulation

of stable forth for one men it indicates the presence of saponins.

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Methodology

5) Test for Lipids

Few drops of 0.5 N alcoholic potassium hydroxide is added to a small quantity of

extracts along with a drop of phenphthalain, the mixture is heated on water both for 1-

2 hour there is formation of soap or partial nutratization of alkali indicates presence of

lipids.

6) Test for carbohydrates

Benedict’s test: Test solution with Benedicts regent and boiled on water both if it

shows reddish brown precipitate.

7) Test for Alkaloids

Hager’s test: Sample solution with Hager’s reagent (saturated picric acid solution)

mixed & allowed to stand. If it gives yellow PPT indicates the presence of alkaloids.

8) Test for Flavonoids:

Ferric chloride test: Sample solution with few drops of Ferric chloride solution

mixed and allowed to stand. If it shows intense green colour indicates the presence of

Flavonoids.

9) Test for Proteins:

Xanthoproteic test: Sample solution treated with concentrated nitric acid and on

boiling if it shows gives yellow precipitate. It indicates the presence of proteins.

Million’s test: Sample solution is added with million’s reagent and heated on a water

bath.

10) Test starch

Anthrone test: Sample solution is added with Anthrone then boiled on water for 10

min. it shows greenish black colour it indicates the presence of stomach.

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Methodology

11) Test for oils:

A small quantity of petroleum ether and benzene extract is pressed separately between

fitter papers if oil stains on the paper indicates is the presence of oils.

Physico chemical analysis of Devadaru

Determination of Foreign matter

100gm of the drug sample is taken and spread it out in a thin layer. The

foreign matter should be detected by inspection with the eye or by the use of lines

(6X) separated and weigh then calculated the % present.

Determination of Total Ash

About 3 gm of the bark powder of drug is taken in tared silica dish ignite it by

dreadyally increasing the heat to 500-6000C until it is white, indicating the absence of

carbon then it is cooled & weighed then calculate the %.

Determination of acid soluble ash

To the crucible containing the total ash add 25 ml of hydrochloric acid cover

with watch glass and boiled gently for 5 minutes collect the insoluble matter in a

cubicla or on an ashen filter paper wash with hot water and ignite calculate the % of

acid soluble ash with reference to the air dried drug.

Determination of water soluble ash

To the crucible containing the total ash, add 25 ml of water and boiled for 5

mins, then collect the insoluble matter in a crucible or on an ashen filter paper, wash

with hot water and ignite for 15 minutes at a temp not exceeding 4500C substract the

weight of the insoluble matter from the height of the ash. The difference in weight

represent the water soluble ash calculate the % of water soluble ash with reference to

the air dried drug.

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Methodology

Determination of Alcohol soluble extractive

Macerate 5 gm of the air dried drug, coarsely powdered with 100 ml of

ethanol (Alcohol) of the specified strength in a closed flask for 24 hrs. shaking

frequency during the first 6 horus and allowed to stand for 18 hrs, thereafter, filter

rapidly, taking precaution against loss of solvent, evaporate 25 ml of the filtrate to

dryness in a tasted flat bottomed shallow dish, and dry at 1050 and weighed calculate

the percentage of Alcohol soluble extract with reference to the air dried drug.

Determination of water soluble extractive

Add 5gm to 50ml of water at 800 in a stopped flask, shaken and allowed to

stand for 10 mins cool add 2 gm of kieselghur and filter, transfer 5 ml of the filtrate to

a tared evaporating dish, 7.5 cm in diameter evaporate the solvent on a water bath,

continue drying for 30 mins finally dry in a steam oven for 2 hours and weigh the

residue calculate the percentage of water soluble extract with reterence of the air dried

drug.

Identification by T.L.C

Drug: Extraction of sample (Aq & Alc) which is treated with 1:10ml solute; solvent

like ethyl alcohol with dilution method.

Equipment: Silica gel, TLC kit, hot air oven, standard glass, wattaman glass plate,

beakers, sprayer.

Chemicals: Dragendroff’s reagent, Silica gel, ethyl alcohol.

Method: T.L.C. of the ethyl alcohol extract of the sample & Aqueous extract of the

sample was carried out as follows.

The silica gel powder mixed with water and made thin paste, then with the

help of glass slide, the silica gel was spread on glass plates uniformly, After some

times the air dried plate were kept in a hot oven at110-120 degree centigrade heay

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Methodology

was given continuously then the prepared sample is kept on a side of the plate then

immersed in solvents upto 30 minutes then Dragendroff’s solution is sprayed on the

plates.

A parameter called the Rf value is always used in TLC this is determined as

follows.

Rf = Distance traveled by the solute

__________________________

Distance traveled by the solvent

Aq extract = 12.6 Alc extract = 12.5

_____ = 0.96 _____ = 0.86

13 14.5

Experimental study

Place of work:

The study was conducted in PG cum Research center D.G.M.A.M.C Gadag.

Preliminary phyto chemical investigations of Devadaru carried out at PG cum

Research center DGAMC Gadag source of animals.

Source of animals:

The required number of Healthy albino rats of either sex were selected for

experimental study and maintained in the animal house. In PG cum Research center

D.G.A.M.C. Gadag.

Housing and feeding of animals:

The animals were maintained at room temperature 250C, with 12 hrs day and

dark cycles, the standard laboratory diet was given with an unlimited supply of

drinking water.

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Methodology

Preparation of animals:

The animals were randomly selected, marked to permit individual

identification and kept in their cages for one week prior to dosing to allow for

acclimation to the lab condition.

Preparation of doses/Vehicle

All the extracts were prepared as a suspension by triturating with distilled

water and with 1% tween20.

Mode of administration

Administration of drug through intra gastric tube using 2 ml disposable

syringe fitted with 20 gauze stainless steel needle provided with suitable smooth

catheter was used for drug administration to avoid injury to the rats.

Pre determined quantities of extracts were mixed with distilled water & 1%

tween 20 (calculated quantity) and suspension was prepared known quantity of

suspension was taken in the syringe & pushed directly.

Calculation of the dose

Rat dose = Human dose X 0.018 X 5

Trial drug: Aqueous extract

Alcoholic extract

20mg/100gm body weight – (Ref Indian journal of Pharmacology (1973) P.No-335)

Conversion of 1Kg body weight

Trial drug A – Aqueous extract - 20mg / 100gm body wt

200mg/Kg body wt

Trail drug B – Alcoholic extract - 20mg / 100 gm body wt

200 mg/ kg body wt

Standard drug

= Human dose X 0.018 X 5

= 1800mg X 0.018 X 5

= 32.4 X 5

= 162 mg / kg body wt

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Methodology

Table 3.1 Protocol of experimental study

1 Sample 24 albino rats of either sex are selected randomly

2 Inclusive criteria Healthy albino rats weight – 150 – 200 gms

3 Exclusive criteria Other wise does not full fill above condition.

4 Groping Each group having 6 rats, kept in separate cage

Group I – Control group 1% normal saline was fed orally to the

albino rats at the dosage of 1 ml each animal in the single dose.

Group II – Standard group Ibuprofen suspension was fed orally

to the albino rats at the dosage of 100 mg/kg body weight.

Group III – Trial group A

Aqueous extract of devadaru is given at the dosage of 200 mg/

kg

Group IV – Trial group B

Alcoholic extract of devadaru is given the dosage of 200 mg/kg.

Table No 3.2 Concentration dose and duration before induction of inflammation

Group Drug or

extract

Dose Route of

administration

Time of

administration

prior to induce

inflammation

Control Group

I

1% Normal

saline

0.2ml /rat Orally 60 min

Standard

Group II

Ibuprofen 162mg/kg Orally 60 min

Trial group A

Group III

Aqueous

extract

200 mg/kg Orally 60 min

Trial group B

Group IV

Alcoholic

extract

200mg / kg Orally 60 min

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Methodology

Procedure111

• Total 24 albino rats were taken for the experimental study and subjected them

in four groups of six rats in each group.

• One hour before inducing inflammation the prepared medicines were

administered orally to the respective groups of rats.

• Then inflammation is induced by injecting 0.1 ml carrageenan into the sub

plantar region of the left hind paw of all the groups.

• Paw volume of all the rats were measured after ½ hr, 1 hr, 2 hr, 3hrs. by using

plethymograph.

• Then compare the anti-inflammatory effect of aqueous & alcoholic extract of

Devadaru with control & standard drug treated groups.

Statistical analysis:

The data collected were statistically analyzed by using unpaired test, paired ‘t’

test – 4 ANOVA with the consultation of biostatistician.

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Results

RESULTS

OBSERVATION AND RESULTS

Observation during Alcoholic extract of Devadaru [Cedrus deodara ]

Observation during Aqueous extract of Devadaru

Preliminary phyto chemical analysis of Devadaru

Physico chemical analysis of Devadaru

All the datas about the parameters considered for the study

Results are compared

Observation regarding the preparation of the drug

The dried stem barks of devadaru were brown in colour with characteristicof

aromatic odour. 2 kg of Devadaru [cedrus deodara] was taken. Out of that we

obtained 1980gms of dried devadaru The dried stem barkswere subjected to

powdering in the pulverizer.The final yield of coarse powder was about 1.8 kg

Observation during preparation of the Alcoholic extract

By appropriate technique the coarse powder of Devadaru is put in the round

fold of filter paper in sauxhlet apparatus. So that it cannot obstruct any path

ways of sauxhlet apparatus.and uniform temperature is maintained.

During each batch, the cycles were continued till up to extractive factors of the

powder were get completely extracted in to the solvent then and then only

every batch was stopped.

After extraction solvents were distilled off

Observation was done so that the solvent is completely distilled off from the

total extraction.

Semisolid extraction taken off and put over the magnetic stirrer for

concentration of extraction should not be so liquid or completely dried.

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Results

500gm of coarse powder of Devadaru yielded about 50gm alcoholic extract

(10%) the alcoholic extract was dark brown in colour with aromatic odour.

Observation during Aqueous extract of Devadaru

200gm of coarse powder of Devadaru (cedrus deodara) yielded about 18gm of

aqueous extract. The aqueous extract was dark brown in colour with aromatic odour.

Observations of Preliminary Phytochemical Test:

1) Test for Sterols:

a) Salkowiski's test

Alc Extract + Conc H2 SO4 Shaken Lower layer turns red.

Indicates the presence of Sterols.

Aq Extract + Conc H2 SO4 Shaken Lower layer does not turns red.

Indicates the absence of sterols.

b) Sulphur test

Alc Extract + Sulphur Powder Shaken Sinks

Indicates the presence of Sterols

Aq Extract + Sulphur Powder Shaken does not Sinks

Indicates the absence of Sterols

2) Test for Triterpenoids:

Salkwoski's test:

Alc Extract+Conc H2 SO4 Shaken lower layer turns to red.

allow to stand

Indicates Presence of Triterpenoid.

Aq Extract+Conc H2 SO4 Shaken lower layer turns to red.

allow to stand

Indicates Presence of Triterpenoid.

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Results

3) Test for Glycosides

Keller Killiani test

Alc Extract+ Glacial acetic acid in + Conc H2 SO4 No separation between two

2ml of ferric chloride

layers

Aq Extract+ Glacial acetic acid in + Conc H2 SO4 No separation between two

2ml of ferric chloride

layers

Indicates absence of Glycosides in both the extracts.

4) Test for Saponin's:

a) Foam test:

Alc Extract+Saponin Shake H2O No Formation of froth.

Indicate the absence of Saponin.

Aq Extract+Saponin Shake H2O No Formation of froth.

Indicate the absence of Saponin.

5) Test for Lipids

Alc Extract+0.5 N alc potassium + a drop of phenolphthalein heated on water bath for

1-2 hrs Shake H2O

formation of soap. Indicates the presence of lipids.

Aq Extract+0.5 N alc potassium + a drop of phenolphthalein heated on water bath for

1-2 hrs Shake H2O

formation of soap. Indicates the presence of lipids.

6) Test for Carbohydrates:

Benedict's test:

Alc extract + Benedict's reagent boil on water bath reddish brown PPT

Indicates the presence of Carbohydrate

Aq extract + Benedict's reagent boil on water bath reddish brown PPT

Indicates the presence of Carbohydrate

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Results

7) Test for Alkaloids:

Acid soln of sample + Hager's reagent Picric acid Observed yellow PPT

saturated

Indicates the presence of Alkaloids in both extracts

8) Test for Flavonoids:

Ferric Chloride test

Alcoholic extract soln +Few drops of Ferric does not shows intense green

Chloride

colour.

Indicates absence of Flavonoid.

Aq extract soln +Few drops of Ferric does not shows intense green colour.

Chloride

Indicates absence of Flavonoid.

9) Test for Tannins:

a) 1 ml alcoholic soln treated with Fecl2 dark precipitate

Indicates presence of Tannin.

b) Alcoholic Soln treated with lead acetate white precipitate

Indicates presence of Tannin.

a) 1 ml Aq soln treated with Fecl2 dark precipitate

Indicates presence of Tannin.

b) Aq Soln treated with lead acetate white precipitate

Indicates presence of Tannin.

10) Test for Proteins:

Xanthoproteic test

Alcoholic extract soln +conc Nitric acid boiling does not shows Yellow PPT

Indicates absence of Proteins

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Results

Aq extract soln +conc Nitric acid boiling shows Yellow PPT

Indicates presence of Proteins

11) Test for Starch:

Alcoholic extract soln +Anthrone boiling on shows Greenish black colour

Water bath

Indicates presence of Starch

Aq extract soln +Anthrone boiling on shows Greenish black colour

Water bath

Indicates presence of Starch

12) Test for Oils:

Oils stains on the filter paper.

Indicates the presence of oil in both the extracts.

Table No. 4.1

Results of Preliminary Phytochemical investigation of Devadaru (Cedrus

deodara)

Chemical Tests Alcholic extract Aqueous extract

Test for Sterols + -

Test for Triterpenoids + +

Test for Glycosides - -

Test for Saponins - -

Test for Lipids + +

Test for Carbohydrates + +

Test for Alkaloids + +

Test for Flavonoids - -

Test for Tannins + +

Test for Resins + +

Test for Proteins - +

Test for Starch + +

Test for Oils + +

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Results

Table No. 4.2

Physico chemical values of Devadaru (Cedrus Deodaru)

Foreign matter 0.23 %

Total Ash 4.1 %

Acid soluble Ash 17.5%

Water soluble Ash 12.5%

Alcoholic soluble extractive 86%

Water soluble extractive 54%

Identification by TLC

About three to six centimeter solvent front migration is sufficient to effect proper

separation Wattman TLC plates produced from 4-5 micro-meter, Silica gel, with an

inert binder to form 200 mm layers about 7 cm development distance was achieved

sample preparation in TLC needs a concentrated solution as very less amount to be

applied and it had been developed using the technique of TLC.

The details of TLC as follows

Table No 4.3

Plate Size : 20 x 8 cm

Technique : One way ascending

Temperature : 30 C

Examination : Day light after spraying

Plate thickness : 3 mm

Activation temperature : 110 C

Time : 30 min- 1 hr

Detecting Spraying Reagent : Dragendroff's reagent

Absorbent Layer : Silica gel G(Activated) percolated plates

Solvent System : Chloroform

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Results

• The Silica gel powder mixed with water and make thin paste ,then with the

help of glass slide the silica was spread on glass plate uniformly.

• After some times the air dried plates are kept in a hot oven at 110 C -120 C

heat was given continuously.

• For one hour then the prepared sample was kept on one of the plate then

immersed in a solvent up to 10 minutes and then Dragendroff's solution is

sprayed on the plates.

During this procedure following observations were observed:

• The Silica gel slurry taken on plates with the help of glass slide, the silica gel

was spread on glass plates uniformly.

• After sometimes the air dried plates were kept in hot oven at 110 C- 120 C.

heat was given continuously.

• After that, the prepared sample was kept inside the developing chamber with

the plate, then immersed in a solvents up to 30 minutes , closing the plate with

the lid.

• After Dragendroff's reagent was sprayed on the plates.

• Black spot was observed on TLC plate.

Results of TLC

Rf = Distance traveled by the Solute

Distance traveled by the solvent

Alc extract Rf = 12.5

= 0.86

14.5

Aq extract Rf = 12.6

= 0.96

13

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Results

Observation of experimental study

Sample size

24 Albino rats were selected for the study

I. Inclusive criteria:

i) Healthy albino rats

ii) Albino rats weighing 150-200 gm

iii) Albino rats between 90-120 days old were included.

II) Exclusive criteria

i) Unhealthy Albino rats

ii) Weighing within 150 & above 200 gm

iii) Albino rats of below 90 days & above 120 days were excluded.

Induction method

The prepared medicines were administered orally to the respective groups of

rats. After 1 hour inflammation is induced by injecting 0.1 ml of carrageenan into the

sub planter region of left hind paw of all the four groups of rats without disturbing the

normal behaviour.

i) Initial paw volume was recorded

ii) Immediately just after the injection of Carrageenan, Intalammation was

recorded

Observation of Anti inflammatory activity

i) The rats were held in a good position where the normal Physiological

functions should not be affected.

ii) The hind paw of the rats should be in the protruding position.

iii) The hind paw should be immersed in a ‘Y’ Shape tube of plethymograph.

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Results

iv) Carrageenan induced hind paw after immersing the mercury level of ‘Y’

shape tube suddenly raised.

v) The raised mercury level was measured in mm

vi) That is the inflammation = raised mercury from ‘Y’ shape tube in mm.

vii) For group I treated with 1% Normal saline after induction of carrageenan

the decreased inflammation was calculated.

viii) For Group II treated with standard drug Ibuprofen suspension after

induction of carrageenan reduction of inflammation was calculated.

ix) For Group III treated with trial drug Aqueous extract after induction of

carrageenan reduction of Inflammation was recorded.

x) For Group IV treated with trial drug Alcoholic extract after induction of

Carrageenan reduction of Inflammation was recorded.

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Results

Master Chart

Group SN Mark Paw Volume Recovery

or death

½ hr 1st hr 2nd hr 3rd hr

1 Head 0.11 0.24 0.31 0.40 Recovered

2 Body 0.12 0.22 0.32 0.42 "

3 Tail 0.11 0.23 0.31 0.44 "

4 Rt ft lb 0.12 0.24 0.33 0.40 "

5 Rt hd lb 0.11 0.23 0.31 0.43 "

1 Control

6 Lt hd lb 0.13 0.24 0.33 0.44 "

1 Head 0.043 0.09 0.14 0.11 "

2 Body 0.042 0.07 0.13 0.10 "

3 Tail 0.041 0.06 0.16 0.10 "

4 Rt ft lb 0.042 0.08 0.14 0.12 "

5 Rt hd lb 0.040 0.08 0.15 0.12 "

2

Standard

6 Lt hd lb 0.042 0.07 0.13 0.10 "

1 Head 0.10 0.21 0.28 0.38 "

2 Body 0.10 0.22 0.29 0.41 "

3 Tail 0.09 0.21 0.28 0.38 "

4 Rt ft lb 0.10 0.21 0.29 0.38 "

5 Rt hd lb 0.11 0.22 0.31 0.39 "

3

Aqueous

extract

200

mg/kg

body wt 6 Lt hd lb 0.10 0.20 0.30 0.39 "

1 Head 0.09 0.12 0.18 0.14 "

2 Body 0.08 0.14 0.19 0.14 "

3 Tail 0.08 0.12 0.18 0.12 "

4 Rt ft lb 0.07 0.12 0.17 0.13 "

5 Rt hd lb 0.08 0.14 0.18 0.12 "

4

Alcoholic

extract

200

mg/kg

body wt 6 Lt hd lb 0.09 0.12 0.18 0.14 "

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Results

Table No. 4.3 Parameter I - Showing the readings of paw volume of all the

groups of Rats after ½ hr

Samples Control group(Group I)

Standard group

(Group II)

Trial group A (Group III)

Trial group B (Group IV)

1 0.11 0.043 0.10 0.09 2 0.12 0.042 0.10 0.08 3 0.11 0.041 0.09 0.08 4 0.12 0.042 0.10 0.07 5 0.11 0.040 0.11 0.08 6 0.13 0.042 0.10 0.09

Table No. 4.4 Summary of Data

S.L.No

Group Samples Mean Standard deviation

Standard error of

mean

Median

1 Control 6 0.116 0.0081 0.0033 0.115 2 Standard 6 0.041 0.0010 0.00042 0.042 3 Trial group A

(Aq extract) 6 0.081 0.0075 0.0030 0.080

4 Trial group B (Alc extract)

6 0.100 0.0063 0.0025 0.100

Table No 4.5 Anova Table

S.L.No

Source of variation

Degree of

freedom

Sum of squares

Mean squares

F Value

1 Treatment 3 0.0187 0.0062 2 Residuals 20 0.00082 4.110 3 Total 23 0.01952 151.66

Table No. 4.6 Comparison

SL.no Comparison Mean difference

t value P value

1 Ct Vs std 0.0750 28.656 p < 0.001 2 Ct Vs Aq 0.016 6.36 p < 0.01 3 Ct Vs Alc 0.0350 13.37 p < 0.001 4 Std Vs Aq - 0.058 22.28 p < 0.001 5 Std Vs Alc - 0.040 15.28 p < 0.001 6 Aq Vs Alc - 0.018 7.005 p < 0.001

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Results

Graph. 1

Paw volume observed in Individual Rat of control group

0.11 0.12 0.11 0.12 0.110.13

0

0.05

0.1

0.15

0.2

0.25

Paw

Vol

ume

1 2 3 4 5 6Rat (Samples)

After 1/2 Hour

Graph. 2

Paw volume observed in Individual Rat of Standard group

0.043 0.042 0.041 0.042 0.04 0.042

0

0.05

0.1

0.15

0.2

0.25

Paw

Vol

ume

1 2 3 4 5 6Rat (Samples)

After 1/2 Hour

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Results

Graph. 3

Paw volume observed in Individual Rat of Trial group A (Aqueous extract)

0.1 0.1 0.09 0.1 0.11 0.1

0

0.05

0.1

0.15

0.2

0.25

Paw

Vol

ume

1 2 3 4 5 6Rat (Samples)

After 1/2 Hour

Graph. 4

Paw volume observed in Individual Rat of Trial group B (Alcoholic extract)

0.09 0.08 0.08 0.07 0.08 0.09

0

0.05

0.1

0.15

0.2

0.25

Paw

Vol

ume

1 2 3 4 5 6Rat (Samples)

After 1/2 Hour

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Results

Table No. 4.7 Parameter II Showing the readings of paw volume of all the

groups of Rats after 1 hr

Samples Control group(Group I)

Standard group

(Group II)

Trial group A (Group III)

Trial group B (Group IV)

1 0.24 0.09 0.21 0.12 2 0.22 0.07 0.22 0.14 3 0.23 0.06 0.21 0.12 4 0.24 0.08 0.21 0.12 5 0.23 0.08 0.22 0.14 6 0.24 0.07 0.20 0.12

Table No. 4.8 Summary of Data

S.L.No

Group Samples Mean Standard deviation

Standard error of

mean

Median

1 Control 6 0.233 0.00816 0.0033 0.235 2 Standard 6 0.075 0.01049 0.0042 0.075 3 Trial group A

(Aq extract) 6 0.211 0.0075 0.0030 0.210

4 Trial group B (Alc extract)

6 0.126 0.0103 0.0042 0.120

Table No 4.9 Anova Table

S.L.No

Source of variation

Degree of

freedom

Sum of squares

Mean squares

F Value

1 Treatment 3 0.09823 0.03274 2 Residuals 20 0.001700 8.500 3 Total 23 0.09993 385.23

Table No. 4.10 Comparison

SL.no Comparison Mean difference

t value P value

1 Ct Vs std 0.158 42.06 p < 0.001 2 Ct Vs Aq 0.021 5.75 P < 0.01 3 Ct Vs Alc 0.106 28.34 p < 0.001 4 Std Vs Aq - 0.13 36.31 p < 0.001 5 Std Vs Alc - 0.051 13.72 p < 0.001 6 Aq Vs Alc - 0.085 22.58 p < 0.001

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Results

Graph. 5

Paw volume observed in Individual Rat of Control group after 1 hour

0.24

0.22

0.230.24

0.230.24

0.2

0.25Pa

w V

olum

e

1 2 3 4 5 6Rat (Samples)

After 1 Hour

Graph. 6

Paw volume observed in Individual Rat of Standard group after 1 hour

0.090.07 0.06

0.08 0.08 0.07

0

0.05

0.1

0.15

0.2

0.25

Paw

Vol

ume

1 2 3 4 5 6Rat (Samples)

After 1 Hour

Anti Inflammatory effect of Devadaru 85

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Results

Graph. 7

Paw volume observed in Individual Rat of Trial group A (Aqueous extract) after

1 hour

0.21 0.22 0.21 0.21 0.220.2

0

0.05

0.1

0.15

0.2

0.25

Paw

Vol

ume

1 2 3 4 5 6Rat (Samples)

After 1 Hour

Graph. 8

Paw volume observed in Individual Rat of Trial group B (Alcoholic extract) after

1 hour

0.120.14

0.12 0.120.14

0.12

0

0.05

0.1

0.15

0.2

0.25

Paw

Vol

ume

1 2 3 4 5 6Rat (Samples)

After 1 Hour

Anti Inflammatory effect of Devadaru 86

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Results

Table No. 4.11 Parameter III Showing the readings of paw volume of all the

groups of Rats after 2 hr

Samples Control group(Group I)

Standard group

(Group II)

Trial group A (Group III)

Trial group B (Group IV)

1 0.31 0.14 0.28 0.18 2 0.32 0.13 0.29 0.19 3 0.31 0.16 0.28 0.18 4 0.33 0.14 0.29 0.17 5 0.31 0.15 0.31 0.18 6 0.33 0.13 0.30 0.18

Table No. 4.12 Summary of Data

S.L.No

Group Samples Mean Standard deviation

Standard error of

mean

Median

1 Control 6 0.318 0.009 0.0040 0.315 2 Standard 6 0.141 0.011 0.0047 0.140 3 Trial group A

(Aq extract) 6 0.291 0.011 0.0047 0.290

4 Trial group B (Alc extract)

6 0.180 0.006 0.0025 0.180

Table No 4.13 Anova Table

S.L.No

Source of variation

Degree of

freedom

Sum of squares

Mean squares

F Value

1 Treatment 3 0.1312 0.0437 2 Residuals 20 0.00205 0.00010 3 Total 23 0.1333 426.28

Table No. 4.14 Comparison

SL.no Comparison Mean difference

t value P value

1 Ct Vs std 0.1767 42.06 p < 0.001 2 Ct Vs Aq 0.026 5.75 P < 0.01 3 Ct Vs Alc 0.138 28.34 p < 0.001 4 Std Vs Aq - 0.150 36.31 p < 0.001 5 Std Vs Alc - 0.038 13.72 p < 0.001 6 Aq Vs Alc - 0.111 22.58 p < 0.001

Anti Inflammatory effect of Devadaru 87

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Results

Graph. 9

Paw volume observed in Individual Rat of Control group after 2 hour

0.31 0.32 0.31 0.33 0.31 0.33

00.05

0.10.15

0.20.25

0.30.35

0.4

Paw

Vol

ume

1 2 3 4 5 6Rat (Samples)

After 2 Hour

Graph. 10

Paw volume observed in Individual Rat of Standard group after 2 hour

0.14 0.130.16

0.14 0.150.13

0

0.05

0.1

0.15

0.2

0.25

Paw

Vol

ume

1 2 3 4 5 6Rat (Samples)

After 2 Hour

Anti Inflammatory effect of Devadaru 88

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Results

Graph. 11

Paw volume observed in Individual Rat of Trial group A (Aqueous extract) after

2 hour

0.28 0.29 0.28 0.29 0.31 0.3

0

0.1

0.2

0.3

0.4

Paw

Vol

ume

1 2 3 4 5 6Rat (Samples)

After 2 Hour

Graph. 12

Paw volume observed in Individual Rat of Trial group B (Alcoholic extract) after

2 hour

0.18 0.19 0.18 0.17 0.18 0.18

0

0.05

0.1

0.15

0.2

0.25

Paw

Vol

ume

1 2 3 4 5 6Rat (Samples)

After 2 Hour

Anti Inflammatory effect of Devadaru 89

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Results

Table No. 4.15 Parameter IV Showing the readings of paw volume of all the

groups of Rats after 3 hr

Samples Control group(Group I)

Standard group

(Group II)

Trial group A (Group III)

Trial group B (Group IV)

1 0.40 0.11 0.38 0.14 2 0.42 0.10 0.41 0.14 3 0.44 0.10 0.38 0.12 4 0.40 0.12 0.38 0.13 5 0.43 0.12 0.39 0.12 6 0.44 0.10 0.39 0.14

Table No. 4.16 Summary of Data

S.L.No

Group Samples Mean Standard deviation

Standard error of

mean

Median

1 Control 6 0.421 0.018 0.0074 0.425 2 Standard 6 0.108 0.0098 0.0040 0.405 3 Trial group A

(Aq extract) 6 0.388 0.011 0.0047 0.385

4 Trial group B (Alc extract)

6 0.131 0.0098 0.0040 0.135

Table No 4.17 Anova Table

S.L.No

Source of variation

Degree of freedom

Sum of squares

Mean squares

F Value

1 Treatment 3 0.492 0.164 2 Residuals 20 0.0033 0.00016 3 Total 23 0.4957 984.63

Table No. 4.18 Comparison

SL.no Comparison Mean difference

t value P value

1 Ct Vs std 0.313 59.45 p < 0.001 2 Ct Vs Aq 0.033 6.82 P < 0.01 3 Ct Vs Alc 0.290 55.02 p < 0.001 4 Std Vs Aq - 0.280 53.12 p < 0.001 5 Std Vs Alc - 0.023 4.42 p < 0.05 6 Aq Vs Alc - 0.25 48.69 p < 0.001

Anti Inflammatory effect of Devadaru 90

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Results

Graph. 13

Paw volume observed in Individual Rat of Control group after 3 hour

0.4 0.42 0.440.4 0.43 0.44

0

0.1

0.2

0.3

0.4

0.5

Paw

Vol

ume

1 2 3 4 5 6Rat (Samples)

After 3 Hour

Graph. 14

Paw volume observed in Individual Rat of Standard group after 3 hour

0.11 0.1 0.10.12 0.12

0.1

0

0.05

0.1

0.15

0.2

0.25

Paw

Vol

ume

1 2 3 4 5 6Rat (Samples)

After 3 Hour

Anti Inflammatory effect of Devadaru 91

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Results

Graph. 15

Paw volume observed in Individual Rat of Trial group A (Aqueous extract) after

3 hour

0.38 0.41 0.38 0.38 0.39 0.39

0

0.1

0.2

0.3

0.4

0.5

Paw

Vol

ume

1 2 3 4 5 6Rat (Samples)

After 3 Hour

Graph. 16

Paw volume observed in Individual Rat of Trial group B (Alcoholic extract) after

3 hour

0.14 0.140.12 0.13 0.12

0.14

0

0.05

0.1

0.15

0.2

0.25

Paw

Vol

ume

1 2 3 4 5 6Rat (Samples)

After 3 Hour

Anti Inflammatory effect of Devadaru 92

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Results

Table No. 4.19 Mean of all the groups for all the parameters

Group Treatment Mean ½ hr

Mean ±

SEM

Mean 1 hr

Mean ±

SEM

Mean 2 hr

Mean ±

SEM

Mean 3 hr

Mean ±

SEM

Recovery

or death

I Control

(Normal

saline)

0.116 ±

0.0033

0.233 ±

0.0033

0.318 ±

0.0040

0.421 ±

0.0074

Recovered

II Standard

(Ibuproten)

0.041 ±

0.0042

0.075 ±

0.0042

0.141 ±

0.0047

0.108 ±

0.0040

"

III Aqueous

extract

200mg/kg

0.081 ±

0.0030

0.211 ±

0.0030

0.291 ±

0.0047

0.388 ±

0.0047

"

IV Alcoholic

extract

200mg/kg

0.100 ±

0.0025

0.126 ±

0.0042

0.180 ±

0.0025

0.131 ±

0.0040

"

Graph. 17

Mean paw volume observed between the Groups

0.116

0.0410.081 0.1

0

0.1

0.2

0.3

Paw

vol

ume

Control Standard Trial Group A(Aq extract)

Trial Group B(Alc extract)

1/2 hour

Anti Inflammatory effect of Devadaru 93

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Results

Graph. 18

Mean paw volume observed between the Groups

0.233

0.075

0.211

0.126

0

0.1

0.2

0.3P

aw v

olum

e

Control Standard Trial Group A(Aq extract)

Trial Group B(Alc extract)

1 hour

Graph. 19

Mean paw volume observed between the Groups

0.318

0.141

0.291

0.18

0

0.1

0.2

0.3

0.4

0.5

Paw

vol

ume

Control Standard Trial Group A(Aq extract)

Trial Group B(Alc Extract)

2 hour

Anti Inflammatory effect of Devadaru 94

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Results

Graph. 20

Mean paw volume observed between the Groups

0.421

0.108

0.388

0.131

0

0.1

0.2

0.3

0.4

0.5

Paw

vol

ume

Contrlo Standard Trial Group A(Aq extract)

Trial Group B(Alc Extract)

3 Hours

Anti Inflammatory effect of Devadaru 95

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Results

Statistical Analysis

The data obtained through the experimental study as shown in the tables bring

analyzed statistically based on the student t-test values as follows

• In the control group the result was non significant with p valuse > 0.10

• In standard group the result was highly significant with p value < 0.0001

• In the trial group (Alcoholic extract) the result was highly significant with p

value 0.001

• Comparison between group I (control) & Group II standard drug Ibuprofen

was highly significant that the control group (significant at 5%)

• Comparison between Group I & Group III. Aqueous extract of Devadaru (G

III) is better than the control group (G I) (Significant at 2%)

• Comparison between Group I & Group IV, Alcoholic extract was highly

significant than the control group.

• Comparison between group II & III standard drug is highly significant group

III is moderately significant.

• Comparison between II & IV both groups are highly significant.

• Comparison between III & IV Alcoholic extract ( G4) was highly significant

than group III.

Therefore by observing all the statistical results it can be ascertained that

Devadaru plays a highly significant role with Alcoholic extract and significant

role with Aqueous extract in reducing inflammation being equally effective as the

standard drug Ibuprofen.

Anti Inflammatory effect of Devadaru 96

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Discussion

DISCUSSION

The title of the present study is “Preliminary phyto chemical investigation and

Anti-inflammatory effect of “Devadaru” on Albino rats” An experimental

study.

This Protocol includes the systemic study of the ideal drug Devadaru,

Phytochemical study for determination of different chemical components in

the trial drug experiment study is done for Anti-inflammatory activity.

In Ayurveda there are so many drugs mentioned under the Anti-inflammatory

property, among them Devadaru (cedrus- deodara) is one of the most potent

anti-inflammatory drug.

The present study is of Phytochemical and experimental study of Devadaru,

with its special reference to anti-inflammatory activity, under this the literature

review, disease review, aims and objects of Devadaru are studied. The

materials & methods observations and results were discussed and concluded.

Shotha, shopha and shwayathu the terms used may be different in different

contexts, but all our acharyas has given much importance to this condition.

They have devoted separate chapters for the description of the Nidana

panchakas and chikitsa,

Shushruta while describing the Nirukti of shopha, “Ekadeshothitha shopha

ityuchyate” meaning oedema arising in any one part of the body is shopha

while describing vishesha laxanas of shopha. He uses the word shwayathu,

which has also been used during description of sarva sara shopha, so it may be

under stood that all the three terms are synonymous.

To understand the disease entity for experiments based on modern science, an

attempt has been made by putting correlation between shotha & inflammation.

Anti Inflammatory effect of Devadaru 97

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Discussion

This is according to the respective explainations of the similarities in their

symptoms.

Inflammation is local response of living mammalian tissues elicited as a

defence reaction in order toeliminate or limit the spread of injurious agents as

well as to remove the consequent necrosed cells & tissues.

A series of phenomenon including increase in the vascular permeability,

accumuolation of exudates and bringing into action of many mediators like the

prosta glandin etc. that play an important role are sent into action.

Till the date a number of studies have been carried out to screen the various

herbs, for anti-inflammatory action to put fourth the alternative diseases.

Herbal remedy which could take the place of the synthetic drug of the new era.

The drug Devadaru mainly grows in north-western himalayas, having the

properties like Tikta, katurasa, Laghu snigda guna, ushna veerya & katu

vipaka.

Stem bark of Devadaru is taken for the present study.

The drug was identified by botanists & faculty members of PG department of

Dravyaguna before beginning the study.

Discussion of Phytochemical analysis

Here the Phytochemical study performed to identify the active chemical

components such as alkaloids, sterols, carbohydrates, tri-terpinods & tannins

etc.

Both Aqueous & Alcoholic extracts of Devadaru were subjected for chemical

texts different chemical constituents such as alkaloids with yellow precipitates

carbohydrates with brick red precipitates, sterols with red precipitates,

Anti Inflammatory effect of Devadaru 98

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Discussion

Triterpenoids with yellow precipitate, Tannins with white precipitate indicates

presence of active components.

Discussion on Identification by TLC method

By following the appropriate methodology of TLC preparation, black spot was

observed on TLC plate. This spot indicates the active chemical components present

inside the diluted solutions.

Discussion on experimental study

The design of the study on inflammation was made on animal experimentation

on Albino rats weighing between 150-200 gms were selected. Four groups

made based on the following pattern.

Group I – Control group 1% normal saline was fed orally to the albino rats at

the dosage of 0.2 ml/200gms body weight each animal in the single dose.

Group II – Standard group: Ibuprofin suspension was purchased and fed orally

to the albino rats at the dosage of 162 mg/kg. Body weight.

Group III – Trial group A – Aqueous extract was weighed and given to trial

group A to all the albino rats at the dosage of 200mg/kg body weight.

Group IV – Trial group B alcoholic extract was weighed and given to trial

group B to all the albino rats at the dosage of 200mg/kg body weight.

Carrageenan 0.1ml was used to induce inflammation in the left hind paw of

all the rats keeping the right paw as control. The paw volume of the rats of

four groups before and after injecting carrageenan inflammation was measured

using plethysmograph, paw volume was measured hourly for three hours after

injecting the carrageenan & observations done to see the paw inflammation.

Inflammation was observed between 15-30 mins after induction of

caurageenan, on the analysis of observations it was found that the albino rats

Anti Inflammatory effect of Devadaru 99

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Discussion

in the control group did not show any improvement by 3 hours but the rats in

the trial group A with aqueous extract have shown good response after 3

hours. Where as trial group B with Alcoholic extract & standard drug group

showed improvement during second and third hour of injecting carrageenan.

Statistical analysis showed that the result in a trial group with alcoholic

extract is almost nearer to that of standard group.

Development of oedema induced by carrageenan is commonly correlated with

the exudative stage of inflammation, one of the important processes of

inflammatory pathology. In the beginning of carrageenan injection there is

sudden elevation of paw volume in relation with histamine mediators, After

one hour the inflammation is increased gradually and was elevated during the

later 3 hours.

This second phase could be due to the liberation of prosto glandin & kninins,

which accompanies leucocytes migration.

Animal experimentation has its limitation in the evaluation of inflammation,

all the symptoms cannot be evaluated as done in clinical study here only the

utseda can be evaluated through the aid of plethismography by which the

reduction of inflammation can be calculated.

All the statistical data and graphs were presented in the tables.

Thus through animal experimentation it was found that Devadaru has highly

significant action as anti-inflammatory drug with alcoholic extraction, where

as moderately significant action with Aqueous extract.

The samprapti of shotha begins by vitiation of kapha, Rakta and pitta which

enter the bahya siras and in turn vitiates the vata located there. Thus sroto

rodha is caused which spreads to the area in the viscinity & shotha results.

Anti Inflammatory effect of Devadaru 100

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Discussion

The drug Devadaru is Tikta in rasa, laghu in guna, ushna veerya & katu

vipaka, ushna veerya is known to act on vata and kapha & tikta rasa reduces

pitta and cleans the rakta, laghu guna also acts antagonistically on kapha, katu

vipak in the drug contracts organic tissues and lessons its secretions and in

practice it is found that the katu effect, some times tend to overlap with anti-

inflammatory activity to some extent.

Thus the gunas of trial drug act all together upon pitta, rakta, kapha during

samprapti vighatana and eventually pacified these, once vitiated pitta, rakta

and kapha are brought to the normal state the vayu gets pecified thus clearing

the sroto rodha relieving shotha.

Anti Inflammatory effect of Devadaru 101

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Conclusion

CONCLUSION

• Review of classical and Modern literaures shows that the trial drug Devadaru

is having significant shothahara property.

• Devadaru is having katu, Tikta rasa, Laghu snigda gunas Ushna veerya and

Katu vipaka.

• Devadaru [Cedrus deodara ] belongs to Coniferae family.

• The useful part stem barks were collected and confirmed.

• Aqueous and Alcoholic extracts were prepared from coarse powder of stem

bark of Devadaru.

• Preliminary phytochemical investigations of both extracts were carried out.

• As per the phytochemical investigations sterols,Triterpenoids, Lipids,

Carbohydrates, Alkaloids, Tannins, Resins, Starch, oils are present in both

extracts.

• Rats were selected randomly weighing between 150-200gm

• 0.1 ml of carrageenan was injected into the sub plantar region of left hind paw

to induce inflammation.

• Aqueous extract 200mg / kg and alcoholic extract 200mg / kg body weight

was given to third and fourth group respectively. Therapeuctic effect for

inflammation was observed in both the groups.

• Inflammation was measured through plethysmograph.

• Shotha manifests as disease it self and also as associated symptom.

• Comparing the results from the control, trial groups especially makes out

inhibition activities of Devadaru in inflammation.

• Aqueours extract of Devadaru (G III) is effective in inhibiting the

inflammation when compared with control group (GI)

Anti Inflammatory effect of Devadaru 102

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Conclusion

• Alcholic extract of Devadaru (G IV) is more efficacious in comparison with

both Aqueous and control group (GI & GIII)

• Statistically trial drug Alcoholic extract & standard drug are equipotent.

• Summarizing the above it is concluded that alcoholic extract of Devadaru (G

IV) is highly significant when compared to aqueous extract (G III).

• It is obvious to document, the Alcoholic extract of Devadaru (G IV) has

showed its extreme utility or significance on the inflammation probably

because of its excellent activity of inhibiting prostaglandin synthesis which is

one of the cause for inflammation.

• As per documented experimental studies and analysis of classical literature it

is also noted the reason for the inhibition of inflammation is possible by the

aid of Tikta rasa & ushna veerya properties of the dravya.

Scope for future study

• The study was conducted with one paradigm i.e carageenan induced, other

paradigm like crotonoil induced granuloma pouch, cotton pellet implantation

method etc. can be tested.

• To assess the claim made on Devadaru in regarding inflammation clinical

study is necessary in all phases.

• To get scientifically based description of histo pathology of cells or tissues

Pharmacological study is necessary.

• Higher Phyto chemical investigations are required for the confirmatory

evaluation of responsible phyto constituents contributing to anti inflammatory

activity.

Anti Inflammatory effect of Devadaru 103

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Summary

SUMMARY

The present dissertation entitled “Priliminary phytochemical investigation and

shothahara (Anti-inflammatory) effect of Devadaru (cedrus deodara) on Albino rats -

An experimental study” Comprises of 7 chapters can be summarized as follows

I) Objectives

II) Review of Literature

a) Drug review

b) Disease review

III) Methodology

IV) Results

V) Discussion

VI) Conclusion

VII) Summary

A part from all these in the part of introduction at the beginning, importance of

Dravya guna branch, significant of herbal plant, preparation necessity for the

assortment of this research work aims and objectives materials and methods and plan

of present study is mentioned.

First chapter objectives at the beginning gives an idea of aims & objectives of

present study and design of present research work.

Second chapter Review of literature consists of literature review of drug

Devadaru & literately review of disease shotha drug review induces both ayurvedic as

well as modern aspect. In Ayurvedic aspect History, synonyms, Guna, Varga, Bheda,

Guna, Karma, Prayojynaga, Matra, Prayoga, vishita yoga etc. all these matter

described.

Anti Inflammatory effect of Devadaru 104

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Summary

In modern drug review classification (division, subdivision, class, subclass,

order family, genus, species) distribution, phytochemestry, therapeutic uses all these

thing are described in detail.

The majority of reference described Devadaru has katu, Tikta rasa Laghu

snigda guna, Ushnaveerya and katu vipaka acts as Deepaka, pachan, Vrana shodhaka,

vranaroopana, shothahara etc because of these reasons one can conceptualize that

drug must be effective in the treatment of shotha & other condition related with it.

Disease review includes both Ayurvedic as well as modern aspect. In

Ayurvedic literature as well as modern aspect. In Ayurvedic literature inflammation

has been described under various terms like shotha, shopha, shwayathu, but all these

terms used in similar meaning because of this reason shotha has more nearer meaning

to the kind of inflammation.

Methodology is the 3rd chapter deals with materials and methods which were

used in present work.

Observations statistical data, statistical analysis & reserves and explained in

4th chapter ie results fifth chapter is the discursion part here discussion of preliminary

phytochemical investigation of Devadaru, TLC experimentation & about results was

done over the experimental & statistical study.

Sixth chapter is by observing and analyzing the results obtained during this

study a conclusion was drawn finally the essence of this dissertation has been

explained in 7th chapter i.e., summary.

Anti Inflammatory effect of Devadaru 105

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Bibilography

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P.103.

98) Ibid

99) Ibid

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K.R Shrikantamurthy editor. Varanasi: Krishnadasa academy; 1995. P.269.

101) Ibid

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25,53 & 54. Brahmananda tripati Varanasi: Choukambha surabharati prakashan:

2001. Pg. 441.

103) Ibid

104) Ibid

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Anti Inflammatory effect of Devadaru 116

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Annexure

ANNEXURE Table 3.1 Protocol of experimental study:

Group Sl.No Dose Paw Volume Recovery or death

½ hr 1st hr 2nd hr 3rd hr 1 2 3 4 5

1 Control

6 1 2 3 4 5

2

Standard (Ibuprofen)

6 1 2 3 4 5

3 Trial Group A Aqueous

extract 200 mg/kg

body wt 6 1 2 3 4 5

4 Trial Group B Alcholic

extract 200 mg/kg

body wt 6

Anti Inflammatory effect of Devadaru 117

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Anti Inflammatory effect of Devadaru