Thymosin alpha 1 attenuates lipid peroxidation and improves fructose-induced steatohepatitis in rats

被引:86
作者
Armutcu, F [1 ]
Coskun, Ö
Gürel, A
Kanter, M
Can, M
Ucar, F
Unalacak, M
机构
[1] Zonguldak Karaelmas Univ, Dept Biochem & Clin Biochem, Fac Med, Zonguldak, Turkey
[2] Zonguldak Karaelmas Univ, Dept Histol & Embryol, Fac Med, Zonguldak, Turkey
[3] Ankara Numune Training & Res Hosp, Ankara, Turkey
[4] Zonguldak Karaelmas Univ, Fac Med, Dept Family Med, TR-67000 Zonguldak, Turkey
关键词
fructose-induced steatosis; oxidative stress; nitric oxide; cytokines; thymosin alpha(1); rats;
D O I
10.1016/j.clinbiochem.2005.01.013
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Objectives: The aim of this study was to investigate the effects of thymosin alpha(1) (T alpha(1)) in rats having fructose-induced steatosis. Fructose leads to experimental steatosis in the liver by exerting its effect on some components of the oxidant/antioxidant system, and on several cytokines (interleukin-1 beta, -2, and -6) in blood. Methods: Twenty-four rats at random were divided into three groups (each group containing eight animals); the control group (C), which received a purified diet; the high-fructose-fed group (F); and the high-fructose-fed and Tal injected group (F + T). After the experimental period of 10 days, liver lipid peroxidation and antioxidant status, and blood IL-1 beta, IL-2, and IL-6 levels were quantified. Results: In comparison with the C group, the F group had a higher nitric oxide (NO) level, xanthine oxidase (XO) activity, and lipid peroxidation, as indicated by concentrations of thiobarbituric acid reactive substances (TBARS), and lower superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in the liver. In the F + T group, these markers were near the values of the control group. In addition, increased IL-1 beta and IL-6 levels were kept at near to normal levels with treatment of T alpha(1), but not IL-2 levels. In the F group, the most consistent findings in the histologic sections of liver tissues were the macrovesicular and microvesicular steatosis. T alpha(1) treatment protected the majority of the liver cells, while minimal macrovesicular and microvesicular steatosis was observed in the remaining cells. Conclusions: These results show that a high-fructose diet in rats leads to hepatic steatosis and a defect in the free radical defense system, and that treatment of T alpha(1) may improve these biochemical and morphologic changes in the fructose-fed rat livers. (c) 2005 The Canadian Society of Clinical Chemists. All rights reserved.
引用
收藏
页码:540 / 547
页数:8
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