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 inﬂammatory diseases such as inﬂammatory bowel disease (IBD) remains unclear. In our study, we investigated the anti-inﬂammatory 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 inﬂammatory parameters as well as oxidative stress were evaluated. The results demonstrated that ascorbic acid signiﬁcantly reduced clinical signs, inﬂammatory 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-κB, COX-2 and iNOS expression in the colonic. Taken together, these findings suggest that ascorbic acid contributes to the reduction of oxidative stress and inﬂammatory response in DSS-induced colitis and exerts the potential to prevent and clinical treatment of inﬂammatory bowel disease.
Keywords: Ascorbic acid; NF-κB; experimental colitis; oxidative stress.