Rampal Singh Negi* and Sher Singh
Background: Inflammatory bowel disease (IBD) is referred as inflammatory and ulcerative disease of small and large intestine and comprises of two different but closely related disease, Crohn’s disease (CD) and Ulcerative colitis (UC), the conditions that result in chronic inflammation of small and/or large intestine. Pathophysiology of IBD involves oxidative stress, inflammation and immune responses, while etiology largely encompasses a compound interaction of genetic factor with environmental or microbial factors.
Objective: Several chemical-induced colitis models are extensively employed on laboratory scale as they exactly mimic morphological, histopathological and symptomatical characters of human IBD. The current study focused on the methodology and rationale of exploiting numerous chemical-induced colitis models for assessing the pathogenesis of IBD.
Method: Relevant literature covers advancement of different animal models produces novel understandings to reveal the initiation and the development of IBD therefore literature from numerous sources on the chemical agents such as Trinitrobenzene sulfonic acid (TNBS), Oxazolone, Dextran sodium sulphate (DSS), Acetic acid, Indomethacin, Carrageenan, Peptidoglycan-polysaccharide (PGPS), Immune complex/Formalin, sodium hydroxide (NaOH) have been recognized and compiled in this review.
Results: The idea of the review is to discuss different models, which help to generate mechanisms underlying progression of IBD as well they are helpful to explore and test the potential of treatment drugs that might be useful in treating pathophysiological changes. The results obtained by the use of such models produce novel examples to investigate the drugs in patients; these models compliment and expand study in humans
Keywords: Crohn’s disease, Ulcerative colitis, inflammation, Oxidative stress, Immune responses.