BIOL 3095 November 2011. Annotated Bibliography By: Angélica M. González Sánchez Student number: 804-11-3354Jian YT, Mai GF, Wang JD, Zhang YL, Luo RC, Fang YX. 2005. Preventive and therapeuticeffects 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 colitismurine models and to compare those effects with the ones of actual treatments for inflammatorybowel disease (IBD). The authors point out that curcumin’s achievements rely on its capacity toinhibit 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 resultswere reliably presented in the article by the use of images and a deep description of theprocesses. Because of the used terminology, it can be deduced that this article is directed towardsa scientific audience, reason why it can be a little hard to understand if the reader isn’tprofoundly familiarized with the topic. However, this article results quite useful for the studiedtheme because of its certain conclusions on curcumin’s proficiency.Salh B, Assi K, Templeman V, Parhar K, Owen D, Gómez A, Jacobson K. 2003. Curcuminattenuates DNB-induced murine colitis. American Journal of Physiology Gastrointestinal andLiver Physiology. 285:G235-G243. This article assesses the effects of curcumin in mice with colitis induced bydinitrobenzene sulfonic acid. It addresses many of the causes of inflammation in colitis and howto offset them with low doses of curcumin. Some of its most significant proficient effects wereshown to be: mice’s weight gain, reduced inflammation in the bowel tissue and its significanteffect 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 bindingof the transcription nuclear factor-kB (NF-kB) to the DNA, which otherwise activates cellularresponse to inflammation. This article shows reliability because of the transcendental datacollected and shown in tables and images. Therefore, it results meaningful in demonstratingcurcumin’s ability as an alternative treatment for inflammatory bowel disease.Yadav VR, Suresh S, Devi K, Seema Y. 2009. Effect of Cyclodextrin Complexation ofCurcumin on its Solubility and Antiangiogenic and Anti-inflammatory Activity in Rat ColitisModel. 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 ratswith colitis induced by dextran sulfate solution. In general, it describes the multiple uses ofcurcumin, 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 acyclodextrin (CD) complex. This complex, because of its lipophilic-hydrophobic inside andhydrophilic 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 ofantiangiogenesis, which reduces inflammation. The most important contribution of this article isthat, by showing its experiments with rat colitis models, it demonstrates curcumin’s capability ofoffsetting the symptoms of colitis and, therefore, situates curcumin as a potential treatment forinflammatory bowel disease in a comprehensible and reliable manner.