Involvement of kallikrein-kinin system in development of experimental ulcerative colitis induced by dextran sulfate sodium in rats

• Published in: Japanese Journal of Pharmacology 2001, Vol.85 (suppl.1), p.112-112
• Main Authors: Kazuhisa Kamata, Izumi Hayashi, Katsuharu Boku, Takeo Saeki, Takashi Ohno, Katsunori Saigenji, Masataka Majima
• Format: Article
• Language: Japanese
• ISSN: 0021-5198

Bradykinin which is one of proinflammatory mediators may be a candidate of inducer of ulcerative colitis (UC). In this study, we investigated the involvement of kallikrein-kinin system in development of experimental UC. Experimental UC was induced in male Sprague-Dawley rats with 5% dextran sulfate sodium (DSS, mol wt 5000) in distilled water as drinking water ad libitum for 7 days. Oral administration of FR 173657, a bradykinin B2 receptor antagonist (p.o., 30mg/kg, twice a day), were started on the day when 5% DSS was given as drinking water (day 0). Rats were killed on day 3, 5, and 7, and the length of the large intestine and hematocrit were determined. The length of the large intestine was significantly shortened with development of colitis together with reductions in hematocrit and body weight. Shortening of the large intestine, and reductions in hematocrit and body weight were significantly suppressed in FR 173657-treated rats compared with vehicle control rats. The development of UC in Brown-Norway-Katholiek rats, which can not generate kinin, was suppressed compared with that in normal Brown-Norway-Kitasato rats. These result suggested that the activation of kallikrein-kinin system was involved in the development of UC.