Methyl helicterate protects against CCl4-induced liver injury in rats by inhibiting oxidative stress, NF-κB activation, Fas/FasL pathway and cytochrome P4502E1 level

被引：110

作者：

Lin, Xing ^{[2
]}

Huang, Renbin ^{[2
]}

Zhang, Shijun ^{[2
]}

Zheng, Li ^{[2
]}

Wei, Ling ^{[2
]}

He, Min ^{[2
]}

Zhou, Yan ^{[2
]}

Zhuo, Lang ^{[2
,3
]}

Huang, Quanfang ^{[1
]}

机构：

[1] Guangxi Univ Tradit Chinese Med, Affiliated Hosp 1, Nanning 530023, Peoples R China

[2] Guangxi Med Univ, Nanning 530021, Peoples R China

[3] Inst Bioengn & Nanotechnol, Singapore 169483, Singapore

来源：

FOOD AND CHEMICAL TOXICOLOGY | 2012年 / 50卷 / 10期

关键词：

Helicteres angustifolia L; Methyl helicterate (MH); Hepatoprotective effect; Carbon tetrachloride; TETRACHLORIDE-INDUCED HEPATOTOXICITY; CARBON-TETRACHLORIDE; PROSTAGLANDIN E-2; ACID; CYCLOOXYGENASE-2; INFLAMMATION; EXPRESSION; MECHANISM; MOUSE;

D O I：

10.1016/j.fct.2012.07.053

中图分类号：

TS2 [食品工业];

学科分类号：

100403 [营养与食品卫生学];

摘要：

This study was designed to investigate the protective effects of the methyl helicterate (MH) isolated from Helicteres angustifolia L against CCl4-induced hepatotoxicities in rats. Liver injury was induced in rats by the administration of CCl4 twice a week for 8 weeks. Compared with the CCl4 group, MH significantly decreased the activities of ALT, AST and ALP in the serum and increased the activities of SOD. GSH-Px and GSH-Rd in the liver. Moreover, the content of hepatic MDA was reduced. Histological findings also confirmed the anti-hepatotoxic characterisation. In addition, MH significantly inhibited the proinflammatory mediators, such as PGE(2), iNOS, COX-2, IL-6, TNF-alpha and myeloperoxidase (MPO). Further investigation showed that the inhibitory effect of MH on the proinflammatory cytokines was associated with the downregulation of NF-kappa B. Besides, MH also markedly decreased the levels of Fas/FasL protein expression and the activities of caspase-3/8, as well as the activity of cytochrome P4502E1 (CYP2E1). In brief, the protective effect of MH against CCl4-induced hepatic injury may rely on its ability to reduce oxidative stress, suppress inflammatory responses, protect against Fas/FasL-mediated apoptosis and block CYP2E1-mediated CCl4 bioactivation. (C) 2012 Elsevier Ltd. All rights reserved.

引用

页码：3413 / 3420

页数：8

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