Silibinin inhibits ethanol metabolism and ethanol-dependent cell proliferation in an in vitro model of hepatocellular carcinoma

被引：39

作者：

Brandon-Warner, Elizabeth ^{[1
,2
]}

Sugg, James A. ^{[2
]}

Schrum, Laura W. ^{[2
]}

McKillop, Iain H. ^{[1
]}

机构：

[1] Carolinas Med Ctr, Dept Gen Surg, Charlotte, NC 28203 USA

[2] Univ N Carolina, Dept Biol, Charlotte, NC 28223 USA

来源：

CANCER LETTERS | 2010年 / 291卷 / 01期

关键词：

Hepatocellular carcinoma; Ethanol; Cytochrome P4502E1; Oxidative stress; Mitogenesis; ADENOSYL-L-METHIONINE; NF-KAPPA-B; ER-BETA; ALCOHOL; CANCER; EXPRESSION; SILYMARIN; PATHOGENESIS; ACTIVATION; GROWTH;

D O I：

10.1016/j.canlet.2009.10.004

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Chronic ethanol consumption is a known risk factor for developing hepatocellular carcinoma (HCC). The use of plant-derived antioxidants is gaining increasing clinical prominence as a potential therapy to ameliorate the effects of ethanol on hepatic disease development and progression. This study demonstrates silibinin, a biologically active flayanoid derived from milk thistle, inhibits cytochrome p4502E1 induction, ethanol metabolism and reactive oxygen species generation in HCC cells in vitro. These silibinin-mediated effects also inhibit ethanol-dependent increases in HCC cell proliferation in culture. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

引用

页码：120 / 129

页数：10

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