Anti-oxidant Effects of Resveratrol on Mice with DSS-induced Ulcerative Colitis

溃疡性结肠炎 结肠炎 白藜芦醇 炎症性肠病 髓过氧化物酶 免疫印迹 谷胱甘肽 免疫学 药理学 化学 医学 胃肠病学 内科学 炎症 生物化学 疾病 基因
作者
Jun Yao,Jianyao Wang,Lei Liu,Yingxue Li,An-Ying Xun,Weisen Zeng,Chunhong Jia,Xiaoxia Wei,Jie Feng,Lei Zhao,Lisheng Wang
出处
期刊:Archives of Medical Research [Elsevier]
卷期号:41 (4): 288-294 被引量:200
标识
DOI:10.1016/j.arcmed.2010.05.002
摘要

Oxidant/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.UC 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-alpha, IL-8, IFN-gamma, p22(phox) and gp91(phox) expression levels were detected using quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR), ELISA, and Western blot analysis.Administration 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-alpha, IL-8, IFN-gamma, p22(phox), and gp91(phox) also decreased significantly in the Res-treated group compared to the colitis control group.Oral administration of Res exerts marked inhibitory effects on UC in mice. Resveratrol may play an important role in preventing DSS-induced oxidative damage.
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