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Open Access Research article

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

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

Author Affiliations

1 Medical research center for Globalization of Herbal Formulation, College of Oriental Medicine, Daegu Haany University, Daegu 706-828, Korea

2 Sunlin University, Pohang, Kyungsangbuk-do 791-712, Korea

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BMC Complementary and Alternative Medicine 2013, 13:64  doi:10.1186/1472-6882-13-64

Published: 18 March 2013

Abstract

Background

Korean 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.

Methods

This 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.

Results

RGE 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.

Conclusions

Our results demonstrate that RGE has the ability to protect cells from AA + iron-induced ROS production and mitochondrial impairment through AMPK activation.

Keywords:
Arachidonic acid; Red ginseng; AMPK; Oxidative stress; Mitochondria