Intestinal anti-inflammatory activity of morin on chronic experimental colitis in the rat
Article first published online: 26 FEB 2002
Alimentary Pharmacology & Therapeutics
Volume 15, Issue 12, pages 2027–2039, December 2001
How to Cite
Gálvez, J., Coelho, G., Crespo, M. E., Cruz, T., Rodríguez-Cabezas, M. E., Concha, A., Gonzalez, M. and Zarzuelo, A. (2001), Intestinal anti-inflammatory activity of morin on chronic experimental colitis in the rat. Alimentary Pharmacology & Therapeutics, 15: 2027–2039. doi: 10.1046/j.1365-2036.2001.01133.x
- Issue published online: 26 FEB 2002
- Article first published online: 26 FEB 2002
Morin, a bioflavonoid with antioxidant properties, shows intestinal anti-inflammatory activity in the acute phase of the trinitrobenzenesulphonic acid model of rat colitis.
To assess the anti-inflammatory activity of morin in the chronic stages of trinitrobenzenesulphonic acid-induced rat colitis.
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 sacrificed every week for 4 weeks. Colonic damage was evaluated macroscopically and microscopically. Different biochemical markers of colonic inflammation were also assayed, including myeloperoxidase activity, leukotriene B4 and interleukin-1β synthesis, glutathione and malonyldialdehyde levels and nitric oxide synthase activity.
The administration of morin facilitated tissue recovery during the 4 weeks following colonic insult with trinitrobenzenesulphonic acid, as demonstrated macroscopically and microscopically, as well as biochemically by a reduction in myeloperoxidase activity. The intestinal anti-inflammatory effect of morin was accompanied by a significant reduction in colonic leukotriene B4 and interleukin-1β levels, improvement in colonic oxidative stress and inhibition of colonic nitric oxide synthase activity.
Morin exerts a beneficial anti-inflammatory effect in the chronic phase of trinitrobenzenesulphonic acid-induced rat colitis through the down-regulation of some of the mediators involved in the intestinal inflammatory response, including free radicals, cytokines, leukotriene B4 and nitric oxide.