AIM:To investigate the effects of melatonin (MT) on theexpression of inducible nitric oxide synthase (iNOS) andcyclooxygenase-2 (COX-2) in rat models of colitis.METHODS:Healthy adult Sprague-Dawlay (SD) rats ofboth sexes,weighing 280±30 g,were employed in thepresent study.The rat models of colitis were induced byeither acetic acid or 2,4,6-trinitrobenzene sulfonic acid(TNBS) enemas.The experimental animals were randomlydivided into melatonin treatment and model control groupthat were intracolicly treated daily with melatonin at dosesof 2.5,5.0,10.0 mg·kg~(-1) and equal amount of salinerespectively from 24 h following induction of colitis in ratsinflicted with acetic acid enema and the seventh day inrats with TNBS to the end of study.A normal control groupof rats treated with neither acetic acid nor TNBS but salineenema was also included in the study.On the 28~(th) day ofthe experiment,the rat colon mucosal damage index(CDMI) was calculated,and the colonic prostaglandin E_2(PGE_2),nitric oxide (NO),as well as the iNOS and COX-2expression were also determined biochemically orimmunohistochemically.RESULTS:CDMI increased to 2.87±0.64 and 3.12±1.12respectively in rats treated with acetic acid and TNBS enema,which was in accordance with the significantly elevatedcolonic NO and PGE_2 contents,as well as the up-regulatedcolonic iNOS and COX-2 expression in both of the two ratmodels of colitis.With treatment by melatonin at the dosesof 5.0 and 10.0 mg·kg~(-1),CDMI in both models of rat colitiswas significantly decreased (P<0.05-0.01),which accordedsynchronously and unanimously with the reduced colonicNO and PGE_2 content,as well as the down-regulatedexpression of colonic iNOS and COX-2.CONCLUSION:Melatonin has a protective effect on colonicinjury induced by both acetic acid and TNBS enemas,whichis probably via a mechanism of local inhibition of iNOS andCOX-2 expression in colonic mucosa, AIM: To investigate the effects of melatonin (MT) on theexpression of inducible nitric oxide synthase (iNOS) andcyclooxygenase-2 (COX-2) in rat models of colitis. METHODS: Healthy adult Sprague-Dawlay (SD) rats ofboth sexes, 280 ± 30 g, were employed in thepresent study.The rat models of colitis were induced byeither acetic acid or 2,4,6-trinitrobenzene sulfonic acid (TNBS) enemas. The experimental animals were randomlydivided into melatonin treatment and model control groupt were were intracolicly treated daily with melatonin at doses of 2.5, 5.0, 10.0 mg · kg -1 and equal amount of salinerespectively from 24 h following induction of colitis in rats inflicted with acetic acid enema and the seventh day in rats with the TNBS to the end of study. A normal control group of rats treated with either acetic or nor TNBS but saline anema was also included in the study. On the 28th (April) of the experiment, the rat colon mucosal damage index (CDMI) was calculated, and the colonic prostaglandin E2 PGE_2), nit ric oxide (NO), as well as the iNOS and COX-2 expression were also determined biochemically or immunohistochemically. RESULTS: CDMI increased to 2.87 ± 0.64 and 3.12 ± 1.12 respectively in rats treated with acetic acid and TNBS enema, which was in accordance with the the significantly elevatedcolonic NO and PGE 2 contents, as well as the up-regulatedcolonic iNOS and COX-2 expression in both of the two rat models of colitis.With treatment by melatonin at the doses of 5.0 and 10.0 mg · kg -1, CDMI in Both models of rat colitis were significantly decreased (P <0.05-0.01), which accorded asynchronously and unanimously with the reduced colonicNO and PGE_2 content, as well as the down-regulatedexpression of colonic iNOS and COX-2.CONCLUSION: Melatonin has a protective effect on colonicinjury induced by both acetic acid and TNBS enemas, which is probably via a mechanism of local inhibition of iNOS and COX-2 expression in colonic mucosa,