Ascorbic acid (AA) has been shown to exert beneficial effects, including mitigating oxidative stress and inhibiting inflammation. However, the preventative effect of vitamin C in chronic in fl ammatory diseases such as in fl ammatory bowel disease (IBD) remains unclear. In our study, we investigated the anti-in fl ammatory effects of AA and possible mechanism involved in inhibiting dextran sulfate sodium (DSS)-induced ulcerative colitis in mice. Male C57BL/6 mice were randomly divided to three groups: control group, DSS group, and DSS plus ascorbic acid treated group. Several clinical and in fl ammatory parameters as well as oxidative stress were evaluated. The results demonstrated that ascorbic acid signi fi cantly reduced clinical signs, in fl ammatory cytokines, myeloperoxidase (MPO) and malonaldehyde (MDA) activities, whereas the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were increased in DSS-induced mice. In addition, ascorbic acid was capable of inhibiting NF-kappaB, COX-2 and iNOS expression in the colonic. Taken together, these findings suggest that ascorbic acid contributes to the reduction of oxidative stress and in fl ammatory response in DSS-induced colitis and exerts the potential to prevent and clinical treatment of in fl ammatory bowel disease.