Protective effect of tryptophan against dextran sulfate sodium- induced experimental colitis.

Turk J Gastroenterol. 2013;24(1):30-5.

Shizuma T, Mori H, Fukuyama N.

Department of Physiology, Tokai University, School of Medicine, Isehara, Kanagawa, Japan. shizuma@is.icc.u-tokai.ac.jp

Abstract

BACKGROUND/AIMS: Little is known about the anti-colitis effect of tryptophan or its metabolites. Here, the protective effect and its mechanism of tryptophan administration on dextran sulfate sodium -induced colitis in mice was studied.

MATERIALS AND METHODS: Twenty C57black6 female mice were equally divided into the control group, and treatment group. The control group received a standard CE-2 diet, while the tryptophan group received a CE-2 diet containing 0.5% l-tryptophan. After one week on this diet, all mice were orally administered a solution of 3.5% dextran sulfate sodium for 12 days to induce colitis. Changes in body weight and bloody stool frequency were monitored during dextran sulfate sodium administration. At 12 days post initial dextran sulfate sodium administration, all mice were sacrificed and the histology of their colonic tissue was examined. The nitrotyrosine levels in colonic tissues in both groups, and nitrate and nitrite levels in the urine of the control group, the tryptophan group and the group of mice without dextran sulfate sodium administration was measured.

RESULTS: The tryptophan group showed significantly attenuated body weight loss, bloody stool frequency and ameliorated histological changes of colitis. While tryptophan treatment significantly reduced nitrotyrosine level in the colonic tissues, there was no significant reduction in urine nitrate and nitrite levels compared with the (dextran sulfate sodium-induced) control group.

CONCLUSION: Tryptophan treatment ameliorated dextran sulfate sodium-induced colitis in this study. One of the anti-colitis mechanisms of tryptophan treatment is attributable to an anti-nitration effect, and may not be via the suppression of nitric oxide generation.

PMID: 23794341

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