Ellagic acid protects hepatocytes from damage by inhibiting mitochondrial production of reactive oxygen species

被引：49
|
作者：
Hwang, Jung Me [1 ]
Cho, Jin Sook [2 ]
Kim, Tae Hyeon [3 ]
Lee, Young Ik [1 ,2 ]
机构：
[1] Korea Res Inst Biosci & Biotechnol, Liver Cell Signal Transduct Lab, Metab Syndrome Res Div, Eoundong 305606, Yusong, South Korea
[2] Lees Biotech Co, Mol Canc Res Div, Taejon 305600, South Korea
[3] Wonkwang Univ, Dept Gastroenterol, Sch Med & Hosp, Iksan 500711, Chonbuk, South Korea
来源：
BIOMEDICINE & PHARMACOTHERAPY | 2010年 / 64卷 / 04期
关键词：
Reactive oxygen species; Ellagic acid; Mitochondrial depolarization; Apoptosis; Concanavalin A; Cytoprotective effect; APOPTOSIS; BETA;
D O I：
10.1016/j.biopha.2009.06.013
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
The aim of this experiment is to investigate the antioxidative and antiapoptotic roles of ellagic (EA) acid in in vitro and in in vivo experiment. We measured protective properties of EA against oxidative stress-induced hepatocyte damage in vitro and Concanavalin (ConA)-induced liver damage in vivo. EA, a potent antioxidant, exhibited protective properties against oxidative stress-induced hepatocyte damage by preventing vitamin k3 (VK3)-induced reactive oxygen species (ROS) productions, apoptotic and necrotic cellular damage and mitochondrial depolarization, which is a main cause of ROS production. EA also protects against cell death and elevation of glutathione (GSH), alanine transaminase (ALT) and asparatate transaminase (AST) in Con A-induced fulminant liver damage in mice. These results show that antioxidant and cytoprotective properties of EA prevent liver damage induced by various type of oxidative stress. (C) 2009 Elsevier Masson SAS. All rights reserved.
引用
收藏
页码：264 / 270
页数：7
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