In¯ammatory bowel disease is a chronic disease of the digestive tract, and usually refers to two related conditions, namely ulcerative colitis and Crohn's disease. The aetiology of in¯ammatory bowel disease remains unknown, although it is believed that an alteration in the intestinal immune system contributes to the in¯ammation that occurs. As in other in¯am-matory processes, in¯ammatory bowel disease is characterized by an up-regulation in the synthesis and release of different pro-in¯ammatory mediators, including reactive oxygen and nitrogen metabolites, eicosanoids, platelet-activating factor and cytokines. 1 All of these mediators contribute to the pathogenic cascade that initiates and perpetuates the in¯ammatory response of the gut. As a consequence, and until its aetiology has been completely elucidated, the best strategy to effectively down-regulate intestinal in¯ammation is to interfere with multiple stages of the in¯ammatory cascade, preferably with a single drug treatment. In fact, the SUMMARY Background: Morin, a bio¯avonoid with antioxidant properties, shows intestinal anti-in¯ammatory activity in the acute phase of the trinitrobenzenesulphonic acid model of rat colitis. Aim: To assess the anti-in¯ammatory activity of morin in the chronic stages of trinitrobenzenesulphonic acidinduced rat colitis. Methods: Rats were rendered colitic by a single colonic instillation of 30 mg of the hapten trinitrobenzenesulphonic acid dissolved in 0.25 mL of 50% ethanol. A group of colitic animals was given morin orally at doses of 25 mg/kg daily. Animals were sacri®ced every week for 4 weeks. Colonic damage was evaluated macroscopically and microscopically. Different biochemical markers of colonic in¯ammation were also assayed, including myeloperoxidase activity, leukotriene B 4 and

The intestinal anti-inflammatory activity of two flavonoids, hesperidin and diosmin, was evaluated in the acute stage of the trinitrobenzenesulfonic acid (TNBS) model of rat colitis. The results obtained showed that pretreatment with diosmin (10 mg/kg) or hesperidin (10 and 25 mg/kg) reduced colonic damage compared to TNBS control rats. This effect was confirmed biochemically by a reduction in colonic myeloperoxidase activity compared to non-treated colitic animals. Colonic glutathione levels in colitic animals were significantly increased after hesperidin or diosmin treatment. Diosmin decreased colonic MDA production and inhibited LTB4 synthesis, whereas hesperidin failed to do so. Conversely, only hesperidin improved colonic fluid absorption, which was impaired in colitic animals. In conclusion, both diosmin and hesperidin were able to prevent colonic inflammation, acting via a mechanism in which protection against oxidative insult may play a role.

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