Chonnam Med J.  2005 Dec;41(3):243-252.

Resveratrol Protects HepG2 and Chang Liver Cells from Oxidative Stress

• Nah HY
• Lee WS
• Joo YE
• Kim HS
• Choi SK
• Rew JS
• Kim SJ
• Jung YD
• Ahn BW
• Park JS
• Shin BA

Abstract

Reactive oxygen species (ROS) can induce hepatotoxicity and trigger apoptosis in the liver. In this study, we investigated the protective effects of resveratrol against oxidative stress in HepG2 and Chang liver cells. Cytotoxicity, intracellular oxidative activity and glutathione (GSH)/glutathione disulfide ratio were measured by MTT assay, DCF-DA (2', 7'-dichlorofluorescin diacetate) and GSH assay, respectively. Lipid peroxidation and protein carbonylation were utilized to detect lipid and protein oxidative damage. Cell cycles were analyzed by flow cytometry. The expressions of cell cycle-related nuclear factors were analyzed by Western blotting. Oxidative stress induced by hydrogen peroxide (200 microM) and ethanol (500 mM) generated ROS, lipid peroxidation, and protein carbonylation, and these were dramatically reduced by resveratrol treatment. Resveratrol also prevented intracellular GSH depletion and cell death induced by oxidative stress. It also inhibited cell proliferation and led to markedly reduced mitotic Cdk (Cdk1) levels in oxidative stressed cells. We conclude that resveratrol effectively protects HepG2 and Chang liver cells from oxidative stress.

Keyword

Resveratrol; Oxidative stress; Hepatocytes

MeSH Terms

Apoptosis
Blotting, Western
Cell Cycle
Cell Death
Cell Proliferation
Ethanol
Flow Cytometry
Glutathione
Hepatocytes
Hydrogen Peroxide
Lipid Peroxidation
Liver*
Oxidative Stress*
Protein Carbonylation
Reactive Oxygen Species
Ethanol
Glutathione
Hydrogen Peroxide
Reactive Oxygen Species