| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 3447231 | Archives of Medical Research | 2010 | 7 Pages |
Background and AimsOxidant/antioxidant balance is suggested to be an important factor for the recurrence and progression of ulcerative colitis (UC). The aim of the study is to investigate the potential protective role of resveratrol (Res) against dextran sodium sulfate (DSS)-induced oxidative damage in colon of mice with UC.MethodsUC was induced in mice by oral administration of synthetic DSS (molecular weight 5000) for 7 days. Mice were divided into normal group, colitis control group, low-dose Res-treated group (RLD-treated group), and high-dose Res-treated group (RHD-treated group). Inhibitory effects of concomitant treatment with Res were assessed daily using a Disease Activity Index (DAI) and severity of histological changes. MDA, MPO, SOD and GSH-PX activity of colonic tissue were determined in colon samples by chemical colorimetry. TNF-α, IL-8, IFN-γ, p22phox and gp91phox expression levels were detected using quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR), ELISA, and Western blot analysis.ResultAdministration of Res significantly inhibited the severity of UC compared to the colitis control group. Colonic tissue MDA and MPO activities decreased significantly in Res-treated groups compared to colitis control groups. Furthermore, colonic tissue SOD and GSH-Px activities increased significantly in Res-treated groups compared to colitis control groups. The expression levels of TNF-α, IL-8, IFN-γ, p22phox, and gp91phox also decreased significantly in the Res-treated group compared to the colitis control group.ConclusionsOral administration of Res exerts marked inhibitory effects on UC in mice. Resveratrol may play an important role in preventing DSS-induced oxidative damage.
