Assessment of Anticolitic Drugs in the Trinitrobenzene Sulfonic Acid (TNBS) Rat Model of Inflammatory Bowel Disease

The pathogenesis of the inflammatory bowel diseases (IBD), which include ulcerative colitis and Crohn’s disease, is still not fully understood. It is likely that proinflammatory cytokine release and derangement of the immune response play a role in the inflammatory processes (1 ,2 ), whereas the roles of a wide range of proinflammatory mediators are currently under investigation. In addition, the release of more ephemeral cytotoxic species such as reactive oxygen species or nitric oxide (NO) and other nitrogen species may also be involved in creating epithelial and microvascular injury (3 –8 ). The expression of the inducible calcium-independent isoform of nitric oxide synthase (iNOS) can be considered as a marker of the inflammatory response in the gut. Thus, the quantities of NO produced by iNOS, either by inflammatory cells or the gut tissue, particularly the epithelium, may be involved in both initial cell injury along with oxygen radical such as superoxide, which forms the injurious peroxynitrite, as well as in the subsequent healing of the tissue injury (3 –8 ).