BIOL 3095 November 2011.Annotated Bibliography

By: Angélica M. González Sánchez Student number: 804-11-3354

Jian YT, Mai GF, Wang JD, Zhang YL, Luo RC, Fang YX. 2005. Preventive and therapeutic effects of NF-kappaB inhibitor curcumin in rats colitis induced by trinitrobenzene sulfonic acid. World Journal of Gastroenterology. 11(12):1747-1752.

This article aims to demonstrate the therapeutic properties of curcumin in induced colitis murine models and to compare those effects with the ones of actual treatments for inflammatory bowel disease (IBD). The authors point out that curcumin’s achievements rely on its capacity to inhibit the production of pro-inflammatory cytokines and to promote the expression of anti-inflammatory cytokines. It also focuses on proving curcumin’s capability of normalizing the NF-kB/IkB pathway which when deregulated causes inflammation, as in IBD. All of these results were reliably presented in the article by the use of images and a deep description of the processes. Because of the used terminology, it can be deduced that this article is directed towards a scientific audience, reason why it can be a little hard to understand if the reader isn’t profoundly familiarized with the topic. However, this article results quite useful for the studied theme because of its certain conclusions on curcumin’s proficiency. Salh B, Assi K, Templeman V, Parhar K, Owen D, Gómez A, Jacobson K. 2003. Curcumin attenuates DNB-induced murine colitis. American Journal of Physiology Gastrointestinal and Liver Physiology. 285:G235-G243.

This article assesses the effects of curcumin in mice with colitis induced by dinitrobenzene sulfonic acid. It addresses many of the causes of inflammation in colitis and how to offset them with low doses of curcumin. Some of its most significant proficient effects were shown to be: mice’s weight gain, reduced inflammation in the bowel tissue and its significant effect on inhibiting and regulating inflammation markers such as myeloperoxidase, pro-inflammatory cytokines, p38 mitogen-activated protein kinases (p38 MAPK), between others. The article also displays the capability of pretreatment with curcumin on inhibiting the binding of the transcription nuclear factor-kB (NF-kB) to the DNA, which otherwise activates cellular response to inflammation. This article shows reliability because of the transcendental data collected and shown in tables and images. Therefore, it results meaningful in demonstrating curcumin’s ability as an alternative treatment for inflammatory bowel disease. Yadav VR, Suresh S, Devi K, Seema Y. 2009. Effect of Cyclodextrin Complexation of Curcumin on its Solubility and Antiangiogenic and Anti-inflammatory Activity in Rat Colitis Model. AAPS PharmSciTech [Internet]. [cited 2009 June 3]; 10(3):752-762. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19495987

The article assesses the effect of the turmeric derived polyphenol, curcumin, in rats with colitis induced by dextran sulfate solution. In general, it describes the multiple uses of curcumin, its properties and also its reduced bioavailability because of its poor solubility.

That’s why the article presents an experiment to increase curcumin’s solubility by making a cyclodextrin (CD) complex. This complex, because of its lipophilic-hydrophobic inside and hydrophilic outside, can create a suitable environment for curcumin’s transference and, therefore, promote its absorbance. The study validates that the Hydroxypropyl Beta Cyclodextrin (HPβCD) complexes of curcumin are the ones with the highest solubility and also have the capacity of antiangiogenesis, which reduces inflammation. The most important contribution of this article is that, by showing its experiments with rat colitis models, it demonstrates curcumin’s capability of offsetting the symptoms of colitis and, therefore, situates curcumin as a potential treatment for inflammatory bowel disease in a comprehensible and reliable manner.