Abstract
<p>Animal model of intestinal inflammation is of paramount significance that aids in discerning the pathologies underlying ulcerative colitis and Crohn’s disease, the two clinical presentations of inflammatory bowel disease. The 2,4,6-trinitrobenzene sulfonic acid (TNBS) colitis model represents one such intestinal inflammation-prototype that is generated in susceptible strains of mice through intra-rectal instillation of compound TNBS. In this paper, we demonstrate the experimental induction of TNBS-mediated colitis in a susceptible strain of ICR mice. This can be done by the following steps: a) acclimation, b) induction and c) observation. TNBS-mouse model provides the information in shortest possible time and simultaneously represents a cost effective and highly reproducible model method of studying the pathogenesis of inflammatory bowel disease.</p><p><strong>Video Clips</strong></p><p><a href="https://youtube.com/v/6MsuIGzH3uA">Acclimation and induction of TNBS</a>: 4.5 min</p><p><a href="https://youtube.com/v/ya66SNwoVag">Observation and drug administration</a>: 1.5 min</p>
Highlights
Inflammatory bowel disease, a chronic inflammatory disease, is considered as a prime causative of gastrointestinal epithelial and mucosal tissue damage, and presents broadly in two clinical variations, ulcerative colitis and Crohn’s disease
Transgenic and gene knockout animal models of ulcerative colitis are used. Both higher and lower animals are used as model (Low et al, 2013). One such efficient model is that of trinitrobenzenesulfonic acid (TNBS) colitis, which is generated through the intra-rectal application of a compound 2,4,6-trinitrobenzene sulfonic acid (TNBS), very well known for its oxidizing and heptenating properties
Ethanol is provided for causing a break in the mucosal barrier such that TNBS could further breach into the epithelial wall
Summary
Inflammatory bowel disease, a chronic inflammatory disease, is considered as a prime causative of gastrointestinal epithelial and mucosal tissue damage, and presents broadly in two clinical variations, ulcerative colitis and Crohn’s disease. Transgenic and gene knockout animal models of ulcerative colitis are used. Both higher (rat, mouse, porcine) and lower (zebrafish, drosophila) animals are used as model (Low et al, 2013). One such efficient model is that of TNBS colitis, which is generated through the intra-rectal application of a compound 2,4,6-trinitrobenzene sulfonic acid (TNBS), very well known for its oxidizing and heptenating properties. Preparation of TNBS: Earlier studies have demonstrated that a dose of TNBS at an amount ranging in between 0.4 mg to 4.0 mg per kg weight of mouse prepared in 30 to 50% of ethanol, was successful in inducing colitis. All procedures in this study were approved by the animal care committee at Yeungnam University
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