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Research ArticleExtracts and Fractions from Edible Roots of Sechium edule(Jacq.) Sw. with Antihypertensive Activity

Galia Lombardo-Earl,1,2 Rubén Roman-Ramos,1

Alejandro Zamilpa,2 Maribel Herrera-Ruiz,2 Gabriela Rosas-Salgado,3

Jaime Tortoriello,2 and Enrique Jiménez-Ferrer2

1 Programa de Doctorado en Ciencias Biológicas y de la Salud, División de Ciencias Biológicas y de la Salud,Universidad Autónoma Metropolitana Iztapalapa, 09340 México, DF, Mexico

2 Centro de Investigación Biomédica del Sur (CIBIS-IMSS), Argentina 1, Colonia Centro, 62790 Xochitepec, MOR, Mexico3 Facultad de Medicina, Universidad Autónoma del Estado de Morelos, Calle Iztaccihuátl Esq. Leñeros S/N, Colonia Volcanes,62350 Cuernavaca, MOR, Mexico

Correspondence should be addressed to Enrique Jiménez-Ferrer; enriqueferrer [email protected]

Received 2 September 2013; Revised 2 March 2014; Accepted 11 March 2014; Published 9 April 2014

Academic Editor: José Luis Rı́os

Copyright © 2014 Galia Lombardo-Earl et al. This is an open access article distributed under the Creative Commons AttributionLicense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properlycited.

Sechium edule is traditionally used in Mexico as a therapeutic resource against renal diseases and to control high blood pressure.The purpose of this work is to evaluate the antihypertensive effect of the hydroalcoholic extract obtained from the roots of this plant,including its fractions and subfractions, on different hypertension models induced with angiotensin II (AG II).The hydroalcoholicextract was tested on an in vitro study of isolated aorta rings denuded of endothelial cells, usingAG II as the agonist; this assay provedthe vasorelaxant effect of this extract. Vagotomized rats were administered different doses of AG II as well as the Hydroalcoholicextract, which reduced blood pressure in 30mmHg approximately; subsequently this extract was separated into two fractions(acetone and methanol) which were evaluated in the acute hypertension mouse model induced with AG II, where the acetonefraction was identified as the most effective one and was subsequently subfractioned using an open chromatographic columnpacked with silica gel. The subfractions were also evaluated in the acute hypertension model. Finally, the extract, fraction, andactive subfraction were analyzed by MS-PDA-HPLC, identifying cinnamic derivative compounds like cinnamic acid methyl ester.

1. Introduction

Sechium edule (Jacq.) Sw. (Cucurbitaceae) is an endemic plantfromMexico known as chayote. It is originally from southernMexico (states of Veracruz, Puebla, and Oaxaca) and wasdomesticated in the valleys of Oaxaca and Tehuacan, Puebla[1]. S. edule is cultivated for alimentary purposes, where thestems and fruits are mainly used, although the roots arespecially appreciated in the east and southeast of Mexico [2].The roots are described as a succulent fibrous tuber witha characteristic flavour [3]. Also, this plant is used in theMexican traditional medicine; in Motozintla, Chiapas, the“Mam” indigenous community employs the chayote plant fortreating symptoms such as severe headaches with ringingears, nervousness, and anxiety, where a decoction of the

leaves is prepared for use as drinking water throughoutthe day [4]. Its use is also reported for the treatment ofrenal and urinary disorders, like bladder or kidney stones,inflammation of the urethra, and difficulty and pain whenurinating, as well as high blood pressure, varicose veins, andvenous insufficiency, among others [5, 6].

There has been little pharmacological research done onS. edule. These studies have reported the hypotensive activityof aqueous and hydroalcoholic extracts from aerial partsof the plant; the treatments were administered orally andintraperitoneally in rats and dogs, respectively [7, 8]. Otherreports have indicated that the hydroalcoholic extract offruits of two varieties of S. edule, which were administeredintravenously in anaesthetized rats, produced effects ondifferent cardiovascular parameters such as lowering blood

Hindawi Publishing CorporationEvidence-Based Complementary and Alternative MedicineVolume 2014, Article ID 594326, 9 pageshttp://dx.doi.org/10.1155/2014/594326

2 Evidence-Based Complementary and Alternative Medicine

pressure and displaying changes on electrocardiographic(ECG) recordings [9]. Nonetheless, the action mechanismsby which these extracts act are not described. Phytochemicalanalysis has been done on the hydroalcoholic extracts of rootsand aerial parts of S. edule plants collected in Italy, wherechemical differences between the two plant organs werereported. The aerial parts contained a high concentrationof luteolin glycosides, while the most significant concentra-tion of apigenin derivatives (C-glycosidic and O-glycosidicbonds) was found in the root extract [10]. The aim of thecurrent study was to evaluate the antihypertensive effect ofS. edule root extract and fractions on two different murinemodels, in which the participation of the extracts as a calciumantagonist is proposed, as well as the possible modulation ofAG II, together with the chemical identification of the activecompounds implicated in the pharmacological activity.

2. Materials and Methods

2.1. Plant Material and Extract Preparation. Sechium edule(Jacq.) Sw. roots and aerial parts were collected in thecommunity of Tuxpanguillo, Veracruz, Mexico (18∘4700.5N and 97∘0017.5W, 1721 meters above mean sea level),during the months of April and May. Plant material wasidentified byAbigail Aguilar-Contreras,M.S., and the IMSSMHerbarium Director (located in National Medical Center,Mexico City). Voucher specimens were stored for futurereference (IMSSM-15549). The roots (R) were dehydratedby freeze-drying and ground in an electric mill (Pulvex)obtaining particles of

Evidence-Based Complementary and Alternative Medicine 3

Meter, Biopac Systems MP 150). In all animals, hexametho-nium chloride (ganglion-blocking agent) was administeredat 0.1 g/kg i.v. dose. After BP stabilization, increasing dosagesof AG II (0.5, 1, and 2𝜇g/kg) were administered to establisha dose dependent curve. BP was recorded every 20 s for8min following each dose. After recording the baseline bloodpressure, three doses of SeRHA were administered (50, 100,and 200mg/kg o.p.). One hour later, BP was measured for aperiod of 5min; immediately, AG II was injected i.v., at thedoses previously given, and BP was measured again.

2.4. Acute Hypertension Induced on Mice with AG II. Basedon the acute high blood pressuremodel proposed by Jiménez-Ferrer et al. (2010) [11] to establish an acute model ofhypertension on mice, it was necessary to determine whichdose of AG II was enough to elevate SBP and DBP over thenormal parameters (120/70mmHg). A dose dependent curvewas done (data not shown). The optimal dose defined was1 𝜇g/kg of AG II (Sigma) by i.v. administration. Subsequentlya bioguided analysis was performed to define which extract(SeRHA, SeRAce, or SeRMeOH, 50mg/kg, o.p.) exhibiteda higher antihypertensive activity. The three extracts wereadministered by o.p., one hour prior to the trial, as wellas Losartan (10mg/kg, o.p.) an AT

1receptor antagonist of

AG II that was used as the positive control. The experimentcontrol group received isotonic saline solution (100 𝜇L/10 g,o.p.). One hour after the treatments, under surgical anaes-thesia (pentobarbital 55𝜇g/kg, i.p.), BP was monitored by anoninvasive BP detector (LE 5002 Storage Pressure Meter,Biopac SystemsMP150); 8 BP lectures were taken to establisha base line, immediately after AG II was administered andthe BP was registered again. At this point, the SeRAce extractwas chosen for the chemical separation by chromatographiccolumn. Representative fractions (R2, R5, R6, R8, R11, R14,R17, and R20) were also tested in this same model.

2.5. In Vitro Aorta Ring Assay. Rats were sacrificed by decap-itation, the thoracic aorta was isolated, cleaned of fat andconnective tissue, and all aortas were denuded of endothe-lium film by gentle mechanical procedure and, finally, cutinto rings of about 4-5mm of width. The rings were tiedto stainless steel hooks with silk thread and immersed into10mL organ baths of Krebs solution at 37∘C and oxygenated(O2/CO2, 95 : 5). A basal tension of 2 g was established for

all tissues, and Biopac Systems TSD 125c equipped withAcqKnowledge software recorded changes in basal tension.KCl (120mM) was administered to determine the maximumcontraction of each prepared aorta.

Sixtymin after stabilizing the tissue, ringswere stimulatedwith different concentrations of AG II (from 1.00 × 10−10 to1.00 × 10

−6M) for 10min and then washed out to removestimulant agent and stabilized for another 30min.The tissueswere preincubated with SeRHA (150 𝜇g/mL, 300 𝜇g/mL, and600𝜇g/mL), respectively. The relaxant effect was determinedby comparison amongmaximum vascular contraction beforeand after addition of samples.

To determine the possible vasorelaxant mechanism (likecalcium antagonism), It was evaluate the effect of calcium

Table 2: Effect produced on systolic and diastolic blood pressure ofvagotomized rats by the administration of angiotensin II (i.v.).

AG II doses𝜇g/kg i.v.

Systolic pressuremmHg ± SD

Diastolic pressuremmHg ± S.D.

0.0 127.7 ± 3.13 55.1 ± 3.270.5 144.3 ± 7.34∗ 70.33 ± 6.15∗

1.0 145.6 ± 12.2∗ 78.3 ± 9.30∗

2.0 153.60 ± 11.0∗ 85.5 ± 15.4∗

Data are presented as means ± SD with 𝑛 = 7. ANOVA and post hocBonferroni test. ∗𝑃 < 0.05 was compared to basal data (0.01mg/kg AG II).

over AG II agonistic activity, the assay consisted of evaluatinga calcium concentration curve inducing vasoconstrictionwith AG II at a specific concentration (1 × 10−6M) and theactivity of SeRHA (200𝜇g/mL, 400 𝜇g/mL, and 800 𝜇g/mL);Nifedipine (calcium channel blocker) was employed as posi-tive control.

2.6. Statistical Analysis. Statistical analysis was carried outwith SPSS 11.0 and based on an analysis of variance (ANOVA)followed by Bonferroni test. A significant difference wasestablished with respect to control group when the 𝑃 valuewas lower than 0.05.

3. Results

3.1. Effect of S. edule Root Extract on Vagotomized Rats withAG II Induced Hypertension. Blood pressure elevation onvagotomized rats was established by a dose dependent curve,as showed in Table 2.

The administration of the different dosages of SeRHAextract was capable of inhibiting the increment of BP whengiven the respective dose of AG II, the effect of which waspreestablished in the dose dependent curve. Figure 1 indicatesthe differential of the decrement of the systolic blood pressure(SBP) and diastolic blood pressure (DBP) when given AG II.Once the highest dose of AG II (2.0𝜇g/kg) is administeredin all three SeRHA treatments, there is a proportional dropin BP. In Figure 1(a) the 200mg/kg dose of SeRHA showeda statistical difference when the 2.0 𝜇g/kg AG II dose wasadministered, decreasing BP in 30mmHg (𝐹(2.93) < 53.06,𝑃 < 0.05) when compared with differential effect (de)induced with the lower dose of AG II (0.5 𝜇g/kg) and SeRHA(50mg/kg). The behaviour of the hypotensive activity fromthe SeRHA 100 and 200mg/kg dose was proportional to theadministration of the AG II dose, making it a dose dependentdrop in SBP, where BP dropped 24mmHg, with a statisticaldifference of both groups of 𝐹(2.93) < 152.96, 𝑃 < 0.05,when compared with differential effect (de) induced withthe lower dose of AG II (0.5 𝜇g/kg) and SeRHA (50mg/kg).This activity could be consistent with the modification of thecardiac output of the animals and this might be the cause whyLozoya et al. [7, 8] saw a modification on the ECG recordingswhen they tested the fruit and leaf extracts.

The modification of DBP is shown in Figure 1(b), wherethe three dosages of SeRHA produced an important effect


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Figure 1: Antihypertensive activity of increasing doses (50, 100,and 200mg/kg i.p.) of SeRHA, in vagotomized rats with ganglionblockage by hexamethonium chloride, pretreated with AG II i.v.Each bar represents the average of the differential of systolic (a) anddiastolic (b) blood pressure with respect to the basal pressure, afterAG II administration. ANOVA, post hoc Bonferroni ∗𝑃 < 0.05,when compared to SeRHA 50 mg/kg represented in white bars (𝑛 =6; mean ± SE).

preventing an increase in DBP when administered the differ-ent AG II doses. These results were more evident than thoseof SBP, since only the 100 and 200mg/kg doses of SeRHA thatwere administered in all three AG II groups showed the mostimportant hypotensive activity compared with the smallestdose of SeRHA and AG II that are exhibited as the whitebars, as well as in the SBP results; the highest dose of AG IIand of SeRHA had the most potent effect, with a fall of DBPof around 25mmHg. The impairment of the increment ofDBP by the SeRHA extract in this model might be associatedwith an AG II antagonist activity, due to the nature of thismodel, where one of the ways to block AG II effect wouldbe the extract interacting with the AT

1receptor for AG II,

since the vagotomization and ganglionic blockage inhibit theBP control mechanisms in general, and the model is inducedby intravenous injection of the agonistic AG II, leaving thismechanism of action as the most prominent to occur.

3.2. Ring Aorta Assay. Figures 2 and 3 show the behaviourof the isolated rat aortas without endothelial cells, under twoconditions of stimulation of vascular smooth muscle. Theresulting contraction is reportedwith regard to themaximumcontraction produced by the administration of KCl.

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Figure 2: Percentages of the contraction of vascular smooth muscleof rat aorta rings stimulatedwith increasing concentrations of AG II,with respect to themaximum effect obtained with KCl, as well as theevaluation of the vasorelaxant effect of the SeRHAextract stimulatedwith AG II.

Figure 2 presents the aorta contraction curve dependenton the increasing concentration of AG II (∙), with a 𝐸max =98%and aEC

50= 8.5×10

−9M. It also shows the effect of threedoses of SeRHA + AG II, 150 𝜇g/mL (⬦), 300 𝜇g/mL (◻), and600𝜇g/mL (×); all three extracts had a statistical differencewith respect to AG II, where the first concentration of SeRHAhad a decrease of 14% of 𝐸max, the second one of 44% of 𝐸max,and the highest concentration diminished the contraction66% of 𝐸max. The EC50 values for the three concentrations ofSeRHA were with an average of 1.5 × 10−8M.

Figure 3 shows the Ca++ concentration curve, stimulatedwith a constant concentration of AG II (1 × 10−6M) (∙). Thecontraction of the aorta was dependent on Ca++ concentra-tion. The AG II 𝐸max value was 98% of contraction with anEC50= 0.0008M. When SeRHA + AG II was administered,

the resulting effect had a statistically significant decreaseof 𝐸max where SeRHA of 200𝜇g/mL (⬦) decreased 20%,400 𝜇g/mL (◻) decreased 48%, and finally the 800 𝜇g/mL (×)concentrations produced a 69% contraction of the aorta withrespect to AG II by itself; the values of EC

50obtained were of

0.003M in average. In this experiment, Nifedipine was usedas a positive control due to its calcium channel blocker effect.

3.3. Bioguided Fractioning of SeRHA, Using the Acute Hyper-tension Mice Model Induced with AG II. Having establishedthe hypotensive activity of the SeRHA extract, it is importantto identify which group of compounds is responsible for thebiological activity. The extract was summited to a chemi-cal separation, and two fractions, SeRAce and SeRMeOHextracts, were obtained.The oral administration of the extractand fractions was able to reduce the blood pressure whileadministering AG II (1.0 𝜇g/kg i.v.) (Figure 4). The mostactive fraction was SeRAce and the complete extract SeRHA,shown by statistical differences for SBP of 𝐹(2.57) < 39.69,𝑃 < 0.05, and for DBP of 𝐹(2.57) < 126.76, 𝑃 < 0.05,


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Figure 3: Percentages of the contraction of vascular smoothmuscle of rat aorta rings stimulated with AG II, in presence ofincreasing concentrations of CaCl

2

with respect to the maximumeffect obtained with KCl, as well as the modulating effect of SeRHAextract on the contraction. Nifedipine was used as a positive controldue to its calcium channel blocker activity.

Table 3: Antihypertensive effect produced by losartan (10mg/kg)and fractions (50mg/kg) obtained from SeRAce, on pretreated micewith AG II (1.0𝜇g/kg, i.v. ).

Treatment Systolic BP mmHg Diastolic BP mmHgVehicle 127.51 ± 3.24 61.14 ± 6.74AG II 146.40 ± 3.01 95.90 ± 8.01R2 133.98 ± 15.86 86.3 ± 14.86R5 122.61 ± 16.43 84.5 ± 18.08R6 132.38 ± 17.87 93.03 ± 20.83R8 138.01 ± 14.84 93.63 ± 13.98R11 119.45 ± 19.85 82.07 ± 16.23R14 109.21 ± 13.94∗ 68.88 ± 12.10∗

R17 109.09 ± 8.73∗ 71.66 ± 14.53∗

R20 122.55 ± 13.15 77.71 ± 10.97Losartan 119.50 ± 11.73 77.45 ± 12.41Data are presented as means ± SD with 𝑛 = 7. ANOVA and post hocBonferroni test. ∗𝑃 < 0.05 is with respect to the negative control (AG II1.0 𝜇g/kg).

when compared to the negative control condition (AG II),with a critical decrease of SBP below the base line values,was established by the vehicle (ISS) group. Both Losartan andSeRMeOH did not achieve significant differences in SBP andDBP compared with SeRHA and SeRAce. Nevertheless, theylowered the BP when compared with the AG II group.

3.3.1. Antihypertensive Activity of SeRAce Fractions. Basedon the pharmacological activity of SeRAce extract, it wasselected for chemical separation by chromatographic column,from which eight fractions (R2; R5; R6; R8; R11; R14; R17;andR20)were chosen based on their chromatographic profileto be evaluated on the acute hypertension mice model(Table 3). Five of the eight fractions presented a decrease

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Figure 4: Bioguided assay of S. edule extracts against AG II agonisticeffect. ANOVA, post hoc Bonferroni ∗𝑃 < 0.05, when compared tothe vehicle represented in white bars (𝑛 = 6; mean ± SE).

in BP when administered AG II; all five fractions had asignificant hypotensive activity on SBP although not all ofthem had the same activity on DBP. Only two fractions (R14and R17) were able to significantly decrease SBP (𝐹(2.11) <92.92; 𝑃 < 0.05) and DBP (𝐹(2.11) < 41.18; 𝑃 < 0.05), witha net effect below the SBP of the ISS group and of the controlgroup Losartan. The hypotensive activity of these extractsand fractions could be related to the phenolic compoundsthat were identified in the chemical characterization donethrough HPLC of the R14 and R17 fractions and SeRHA aswell as for SeRAce extracts.

3.4. Chemical Analysis. SeRHA, SeRAce, and the most activefractions (R14 and R17) were analysed by HPLC and MS-PDA-HPLC; the compounds in each one displayed diverseUV spectra that can be related to flavones (𝜆max = 340 nm)and cinnamic acid derivatives (𝜆max = 290 nm).

The extraction made with acetone from SeRHA allowedus to obtain a less polar fraction that also presented theantihypertensive activity that was tested in the biologicalmodel used.

The chromatographic comparison of SeRHA extract withthe fraction SeRAcet that was read at 340 nm (specific forvitexin and other related flavonoids) (Figure 5(a)) allowsobserving the loss of this type of compounds in the fractionSeRAcet as well as the more polar compounds that came outwith the solvent front. When the comparison of these two


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Figure 5: Chromatograms of SeRHA extract (blue line) compared with SeRAcet (black line); they were read at two length waves, panel (a) at290 nm and panel (b) at 340 nm. Fractions R14 (black line) and R17 (blue line) represented in panels (c) and (d) read at 340 nm and 290 nm,respectively, show two peaks (1 and 2) with retention times of 7.21 and 8.04min. Peak 2 corresponds to the cinnamic acid methyl ester thatcorresponds to the MS-PDA-HPLC analysis represented in Figure 6(a) peak 4 and Figure 6(b) peak 160.3.

was analysed at 290 nm (Figure 5(b)), It can be appreciatedan increment in the concentration of the peaks presentthroughout minute 7 to 18 of the retention times of thisfraction. The chemical separation of these fraction derived20 fractions, from which two of them, R14 and R17 (at adose of 50mg/kg), presented significant statistical differencein the biological activity superior to Losartan.These fractionswere compared in the chromatographic method at 290 nm,observing an increment in the peaks with retention time 7.21and 8.04min in both fractions having the sameUV spectrumfor both retention times, peak 1 and 2 from Figures 5(c) and5(d), respectively. TheMS-PDA-HPLC analysis from SeRHAand the Fraction 14 (Figure 6(a)) allowed establishing that

the peak with retention time of 10.8min corresponds to acinnamic acid methyl ester.

4. Discussion

Blood pressure is a mechanism that an organism has tomaintain a constant irrigation of blood, for nutrient distri-bution and oxygenation of organs and tissues. It is regulatedessentially throughout two factors, cardiac output (CO) andtotal peripheral resistance (TPR).The CO is the total amountof blood pumped in to the aorta each minute by the heartand the TPR or vascular resistance is the impediment toblood flow in a vessel. The pharmacological model used in


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this work has the purpose of simulating an alteration in theTPR, increasing blood pressure by the administration of AGII, and triggering a general vasoconstriction reaction. Drugdiscovery [12] describes this assay as an AG II antagonismmodel.

The vagotomization of the rats eliminates the cardio-vascular reflexes, without interfering with the heart rateand normal blood pressure, allowing AG II to induce anincrease of blood pressure, inciting an acute vasoconstrictionwhen administered intravenously without any interventionof the sympathetic and parasympathetic response, whichare responsible for the immediate homeostatic control ofblood pressure. The ganglionic-blockade purpose is to blockthe transmission of nerve impulses through the autonomicganglia [13], impairing the vasculature to compensate bloodpressure when administered AG II or the extract evaluated.

The results obtained from this model allowed us notonly to confirm the antihypertensive effect of this plantbut also to identify the probable action mechanism. Theextracts of S. edule may have an AG II antagonism activity.This action mechanism can be modulated through directantagonism of the AG II receptor AT

1or by the intervention

on calciumfluxes activated byAG II, impeding the immediatevasoconstriction response to the i.v. administration of AG II.

In the isolated aorta assay AG II vasoconstriction actionwas dependent on Ca++ concentration, where it was observedthat the increment in Ca++ promoted a rise of the contractionof the aorta when a single concentration of AG II wasadministered. Nifedipine was used as a pharmacologicalcontrol; it specifically blocks L-type calcium channels as acompetitive antagonist [14] on the calcium influx that canbe through depolarization or by receptor-response coupling[15], which, in this assay, was triggered by AG II. The SeRHA

extract, in comparison to Nifedipine, responded as an irre-versible antagonist (also called pharmacologic antagonist)that shifts the dose-response curve downward, indicating thatthe agonist can no longer exertmaximal effect at any dose. Allthree concentrations of the extract that were tested not onlyinhibited the aorta contraction but also altered the EC

50as a

competitive antagonist would do [16].This behaviour confirms the AG II antagonist effect,

although it could also have a calcium antagonist effect.The activity of SeRHA extract can be associated with anAG II receptor blocking action, as well as obstructing thesecondmessenger system initiated by AG II, which promotesthe efflux of sarcoplasmic calcium that activates the storeoperated channels (SOC) that allows more calcium to enterthe cell and form a calcium-calmodulin complex That endsin vascular contraction [17, 18].

With these results, the antihypertensive and vasorelaxantactivity of S. edule root extract were demonstrated; therefore,a chemical separation was carried out, obtaining a firstfraction SeRAce, whichwas summited to chemical separationand the most chemically relevant fractions obtained wereanalysed on the acute hypertensive model; two of them hadthe most pharmacological activity (R14 and R17) and werethen analysed by HPLC as well as SeRHA and SeRAce. Thechemical results allowed us to identify most polyphenoliccompounds like flavonoids and phenylpropanoids. Vitexinwas identified in SeRHA and SeRAce as well as coumaric andcinnamic acid; in contrast with the extracts, fractions R14 andR17 predominantly had coumaric and cinnamic acid. Thisinformation is relevant and consistent to the results obtainedfrom the pharmacological experiments.

Polyphenolic compounds have a very wide and importantbiological activity regarding cardiovascular diseases. Mainlyin the regulation of high blood pressure, recent studies areevoked on inflammation and ROS scavenging properties ofthis type of compounds [19–22].Thus, there have been studieson flavonoids and cinnamic acid derivative on their calciumantagonism and vasorelaxant activity [23, 24].

Liew et al. [25] demonstrated that red wine polyphenolslike resveratrol act as calcium channel antagonists loweringfree intracellular Ca++. Summanen et al. [23] presented thatnumerous simple phenolic compounds like cinnamic acidderivatives and flavonoids have a potent inhibition of Ca++entry by highK+-evoked activity; the effects were comparableto those of verapamil. They presented an inhibitory activityagainst Ca++ entry similar to the one of another classof natural Ca++ channel antagonists, like furanocoumarinsidentified by Vuorela et al. [26]. Other studies of extracts ofGentiana floribunda that contained flavonoids and tanninsamong other compounds were effective for lowering bloodpressurewith a vasorelaxant effect,mediated by the inhibitionof Ca++ influx via membranous calcium channels and itsrelease from the intracellular stores [27].

The presence of cinnamic acid derivatives in the S.edule extracts and fractions could be responsible for theangiotensin II and calcium antagonist effect, which wereestablished with the pharmacological assays, which aredesigned to identify a specific action mechanism. Cinnamicacid derivatives are a group of natural compounds that have


been studied in different antihypertensive models, mostly asanti-inflammatory and antioxidant activity, although thesestudies are based on chronic hypertension assays, whichoriginate by the alterations of Ca++ fluxes in the vascularsmooth muscle and on the renin—angiotensin—aldosteronesystem.

5. Conclusions

In conclusion the results obtained in this work demonstratethat S. edule extracts have an antihypertensive activity, whichis consistentwith the traditional use inMexico.Thus, the phy-tochemical analysis was not precise on a specific compoundand the richness in polyphenols opens a new range of inquiryfor other action mechanisms of S. edule extracts related toinflammation and oxidative stress damage that is related tohypertension and endothelial dysfunction.

Conflict of Interests

The authors declare that there is no conflict of interestsregarding the publication of this paper.

Acknowledgments

This work was partially supported by CONACyT México(SNI/32291/52834-M), IMSSMéxico (FIS/IMSS/PROT/348),and CONACyT México (Salud/113632) Grants. This paperis taken in part from the Ph.D. of Galia Lombardo Earl(Programa de Doctorado en Ciencias Biológicas y de laSalud) belonging to the Universidad Autónoma Metropoli-tana (UAM), with a Doctoral fellowship from CONACyT,México (Registry no. 208601/202091).

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Research Article Extracts and Fractions from Edible Roots ...downloads.hindawi.com/journals/ecam/2014/594326.pdf · Research Article Extracts and Fractions from Edible Roots of Sechium