The aim of this study was to evaluate the effect of naringin on experimentally induced inflammatory bowel disease in rats.Naringin(20,40 and 80 mg/kg) was given orally for 7 days to Wistar rats before induction of colitis by intrarectal instillation of 2 mL of 4%(v/v) acetic acid solution.The degree of colonic mucosal damage was analyzed by examining mucosal damage,ulcer area,ulcer index and stool consistency.Intrarectal administration of 4%acetic acid resulted in significant modulation of serum alkaline phosphatase,lactate dehydrogenase,superoxide dismutase(SOD),glutathione(GSH),malondialdehyde(MDA) and myeloperoxidase(MPO) content along with colonic nitric oxide(NO),xanthine oxidase(XO) level and protein carbonyl content in the colonic tissue as well as in blood.Naringin(40 and 80 mg/kg) exerted a dose dependent(P < 0.05) ameliorative effect,as it significantly increased hematological parameter as well as colonic SOD and GSH.There was a significant(P < 0.05)and dose dependant inhibition of macroscopical score,ulcer area along with colonic MDA,MPO activity by the7 days of pretreatment of naringin(40 and 80 mg/kg).Biochemical studies revealed a significant(P < 0.05) dose dependant inhibition in serum alkaline phosphatase(ALP) and lactate dehydrogenase(LDH) levels by pretreatment of naringin.Increased levels of colonic NO,XO,protein carbonyl content and DNA damage were also significantly decreased by naringin pretreatment.The findings of the present investigation propose that naringin has an anti-inflammatory,anti-oxidant and anti-apoptotic potential effect at colorectal sites as it modulates the production and expression of oxidative mediators such as MDA,MPO,NO and XO,thus reducing DNA damage. The aim of this study was to evaluate the effect of naringin on experimentally induced inflammatory bowel disease in rats. Naringin (20, 40 and 80 mg / kg) was given orally for 7 days to Wistar rats before induction of colitis by intrarectal instillation of 2 mL of 4% (v / v) acetic acid solution. The degree of colonic mucosal damage was analyzed by examining mucosal damage, ulcer area, ulcer index and stool consistency. Intrarectal administration of 4% acetic acid resulted in significant modulation of serum alkaline phosphatase , lactate dehydrogenase, superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA) and myeloperoxidase (MPO) content along with colonic nitric oxide (NO), xanthine oxidase (XO) level and protein carbonyl content in the colonic tissue as well as in blood. Naringin (40 and 80 mg / kg) exerted a dose dependent (P <0.05) ameliorative effect, as it significantly increased hematological parameter as well as colonic SOD and GSH. dependant inhibit ion of macroscopical score, ulcer area along with colonic MDA, MPO activity by the 7 days of pretreatment of naringin (40 and 80 mg / kg). Biochemical studies revealed significant (P <0.05) dose dependant inhibition in serum alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) levels by pretreatment of naringin. Increased levels of colonic NO, XO, protein carbonyl content and DNA damage were also significantly decreased by naringin pretreatment. The findings of the present investigation propose that that naringin has an anti-inflammatory, anti -oxidant and anti-apoptotic potential effect at colorectal sites as it modulates the production and expression of oxidative mediators such as MDA, MPO, NO and XO, thereby reducing DNA damage.