Red ginseng abrogates oxidative stress via mitochondria protection mediated by LKB1-AMPK pathway

BMC Complementary and Alternative Medicine

Research Article

Eun Jeong Jang¹  Young Woo Kim¹  Guang-Zhi Dong¹  Il Je Cho¹  Sang Chan Kim¹  Sun-Dong Park¹  Seung Ho Kang² 

[1] Medical research center for Globalization of Herbal Formulation, College of Oriental Medicine, Daegu Haany University, 706-828, Daegu, South Korea;Sunlin University, 791-712, Pohang, Kyungsangbuk-do, South Korea;

关键词: Arachidonic acid;    Red ginseng;    AMPK;    Oxidative stress;    Mitochondria;   

DOI  :  10.1186/1472-6882-13-64

 received in 2012-09-13, accepted in 2013-02-26,  发布年份 2013

来源: Springer

【 摘 要 】

BackgroundKorean ginseng (Panax ginseng C.A. Meyer) has been used as a botanical medicine throughout the history of Asian traditional Oriental medicine. Formulated red ginseng (one form of Korean ginseng) has been shown to have antioxidant and chemopreventive effects.MethodsThis study investigated the cytoprotective effects and mechanism of action of Korean red ginseng extract (RGE) against severe ROS production and mitochondrial impairment in a cytotoxic cell model induced by AA + iron.ResultsRGE protected HepG2 cells from AA + iron-induced cytotoxicity by preventing the induction of mitochondrial dysfunction and apoptosis. Moreover, AA + iron-induced production of ROS and reduction of cellular GSH content (an important cellular defense mechanism) were remarkably attenuated by treatment with RGE. At the molecular level, treatment with RGE activated LKB1-dependent AMP-activated protein kinase (AMPK), which in turn led to increased cell survival. The AMPK pathway was confirmed to play an essential role as the effects of RGE on mitochondrial membrane potential were reversed upon treatment with compound C, an AMPK inhibitor.ConclusionsOur results demonstrate that RGE has the ability to protect cells from AA + iron-induced ROS production and mitochondrial impairment through AMPK activation.

【 授权许可】

Unknown   
© Dong et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.