Effect of taurine on oxidative stress and apoptosis-related protein expression in trinitrobenzene sulphonic acid-induced colitis

被引:81
作者
Giris, M. [1 ]
Depboylu, B. [1 ]
Dogru-Abbasoglu, S. [1 ]
Erbil, Y. [2 ]
Olgac, V. [3 ]
Alis, H. [2 ]
Aykac-Toker, G. [1 ]
Uysal, M. [1 ]
机构
[1] Istanbul Univ, Istanbul Fac Med, Dept Biochem, TR-34093 Istanbul, Turkey
[2] Istanbul Univ, Istanbul Fac Med, Istanbul, Turkey
[3] Istanbul Univ, Inst Oncol, Dept Oncol Pathol, Istanbul, Turkey
关键词
apoptosis; oxidative stress; rat; taurine; TNBS-induced colitis;
D O I
10.1111/j.1365-2249.2008.03599.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 [免疫学];
摘要
Ulcerative colitis (UC) is a multi-factorial inflammatory disease of the colon and rectum. The present study was undertaken to investigate the effect of taurine, an anti-oxidant amino acid, on oxidative stress and the expression of apoptosis-related proteins, pro-apoptotic Bax and anti-apoptotic B cell lymphoma-2 (Bcl-2) in colon tissue in rats with 2,4,6-trinitrobenzene sulphonic acid (TNBS)-induced colitis. Rats received taurine (1.5% w/v) in drinking water for 15 days before and 15 days after administration of TNBS solution. Then, colonic myeloperoxidase (MPO) activity, malondialdehyde (MDA) and glutathione (GSH) levels, and Bax and Bcl-2 expression were measured. TNBS-induced colitis caused significantly increased MPO activity and MDA levels and decreased GSH levels in colon tissue compared to controls. Increase in Bax expression and decrease in Bcl-2 expression were detected in colon of rats with TNBS-induced colitis. Taurine treatment was associated with amelioration in macroscopic and microscopic colitis scores, decreased colonic MPO activity and MDA levels and increased GSH levels in TNBS-induced colitis. In addition, taurine reduced the expression of Bax and prevented the loss of Bcl-2 proteins in colon tissue of rats with TNBS-induced colitis. The results of this study show that taurine administration may exert beneficial effects in UC by decreasing inflammatory reactions, oxidative stress and apoptosis.
引用
收藏
页码:102 / 110
页数:9
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