1. 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.

2. 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.