Inflammatoryboweldisease(IBD)isachronicinflammatoryconditionwithanunknownetiology.Nicorandil,apotassiumchannel opener, has been used for many years for the treatment of angina. Recently, it has been shown that nicorandil possesses some novel traits such as anti-apoptotic, gastroprotective, free radical scavenging, and anti-inflammatory properties. Therefore, we set out to examine the possible beneficial effect of nicorandil in a rat model of IBD. Colitis was induced by rectal administration of 2,4,6-trintrobenzene sulphonic acid (TNBS) into rats. Groups of animals used in this study were sham, control, and exposure to dexamethasone,nicorandil,glibenclamid(apureadenosinetriphosphatesensitivepotassiumchannel(KATP)blocker),ornicorandilplus glibenclamid.Drugswereadministeredbygavageandanimalsweresacrificedafter7days.Biochemicalmarkers,includingTNF-αand IL-1β,ferricreducing/antioxidantpower(FRAP),myeloperoxidase(MPO)activityandthiobarbitoricacid-reactivesubstance(TBARS), weremeasuredinthehomogenateofcolonictissue.Resultsindicatethatnicorandilsignificantlyreducesmacroscopicandhistological damageinducedbyTNBS.NicorandildiminishesMPOactivityandlevelsofTBARS,TNF-α,andIL-1βindamagedcolonictissuewith aconcomitantincreaseinFRAPvalue(P<0.01).Theseeffectswerenotreversedbycoadministrationofglibenclamide.Inconclusion, nicorandilisabletoameliorateexperimentalIBDwithadoseinwhichitdoesnotshowanyanti-hypertensiveeffect,andthemechanism ofwhichispartiallyortotallyindependentfromKATPchannels.Itishypothesizedthatnitricoxidedonationandfree-radicalscavenging propertiesofnicorandilupregulateendothelialnitricoxidesynthasemayberesponsibleforthisphenomenon.Thesefindingssuggest thatnicorandilcanbeusefulintreatmentofIBD,althoughfurtherinvestigationsareneededtoelucidatethemechanismsinvolved.