期刊
TOXICOLOGY AND APPLIED PHARMACOLOGY
卷 242, 期 3, 页码 318-325出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.taap.2009.11.005
关键词
Carbon tetrachloride; Oxidative stress; Cytokine; Chemokine; Inflammation
资金
- Korean government (MEST) [50039-2009]
The aim of the present study was to evaluate immunomodulator ginsan, a polysaccharide extracted from Panax ginseng, oil carbon tetrachloride (CCl4)-induced liver injury. BALB/c mice were injected i.p. with ginsan 24 h prior to CCl4 administration. Serum liver enzyme levels, histology, expression of antioxidant enzymes, and several cytokines/chemokines were subsequently evaluated. Ginsan treatment markedly suppressed the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, and hepatic histological necrosis increased by CCl4 treatment. Ginsan inhibited CCl4 induced lipid peroxidation through the cytochrome P450 2E1 (CYP2E1) downregulation. The hepatoprotective effect of ginsan was attributed to induction of anti-oxidant protein contents, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPX) as well as restoration of the hepatic glutathione (GSH) concentration. The marked increase of proinflammatory cytokines (IL-1 beta, IFN-gamma) and chemokines (MCP-1, MIP-2 beta, KC) in CCl4 treated mice was additionally attenuated by ginsan, thereby preventing leukocyte infiltration and local inflammation. Our results suggest that ginsan effectively prevent liver injury, mainly through downregulation of oxidative stress and inflammatory response. (C) 2009 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据