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Int J Clin Exp Med. 2015 Nov 15;8(11):20245-53. eCollection 2015.

Ascorbic acid ameliorates oxidative stress and inflammation in dextran sulfate sodium-induced ulcerative colitis in mice.

Author information

  • 1Department of Gastroenterology, Zhengzhou Children's Hospital Zhengzhou 450053, Henan Province, China.
  • 2School of Pharmacy, Zhengzhou University Zhengzhou 450001, Henan Province, China.
  • 3Department of Emergency, Zhengzhou Children's Hospital Zhengzhou 450053, Henan Province, China.

Abstract

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

PMID:
26884937
PMCID:
PMC4723782
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