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Volume 41, Issue 4, Pages 288-294 (May 2010)


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

Jun Yaoa, Jian-Yao Wangb, Lei Liub, Ying-Xue Lia, An-Ying Xunc, Wei-Sen Zengd, Chun-Hong Jiad, Xiao-Xia Weia, Ju-Ling Fenga, Li Zhaod, Li-Sheng WangaCorresponding Author Informationemail address

Received 1 November 2009; accepted 27 April 2010.

Background and Aims

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.

Methods

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-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.

Result

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-α, IL-8, IFN-γ, p22phox, and gp91phox also decreased significantly in the Res-treated group compared to the colitis control group.

Conclusions

Oral administration of Res exerts marked inhibitory effects on UC in mice. Resveratrol may play an important role in preventing DSS-induced oxidative damage.

(ARCMED-D-09-00538)

a Department of Gastroenterology, Jinan University of Medical Sciences, Shenzhen Municipal People's Hospital, Shenzhen, Guangdong Province, China

b Department of General Surgery, Shenzhen Municipal People's Hospital, Jinan University of Medical Sciences, Shenzhen, Guangdong Province, China

c Department of Gastroenterology, Peking University Shenzhen Hospital, Shenzhen, Guangdong Province, China

d Department of Cell Biology, Southern Medical University, Guangzhou, Guangdong Province, China

Corresponding Author InformationAddress reprint requests to: Li-Sheng Wang, Department of Gastroenterology, Shenzhen Municipal People's Hospital, Jinan University of Medical Sciences, 1017 East Gate Road, Shenzhen, 518020, Guangdong Province, China; Phone: 0086-755-25533018; FAX: 0086-755-25533497

PII: S0188-4409(10)00103-7

doi:10.1016/j.arcmed.2010.05.002


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