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KMID : 1007520100190010207
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Food Science and Biotechnology
2010 Volume.19 No. 1 p.207 ~ p.212
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Korean Red Ginseng Attenuates Hepatic Lipid Accumulation via AMPK Activation in Human Hepatoma Cells
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Quan Hai-Yan
Yuan Hai-Dan
Kim Do-Yeon
Ya Zhang
Chung Sung-Hyun
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Abstract
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In this study, we examined Korean red ginseng (KRG) extract affects on the lipid metabolism in HepG2 cells. Increase in AMP-activated protein kinase (AMPK) phosphorylation was observed when the cells were treated with KRG. Activation of AMPK was also demonstrated by measuring the phosphorylation of acetyl-CoA caboxylase (ACC), a substrate of AMPK. KRG down-regulated gene expressions of sterol regulatory element binding protein 1c (SREBP1c) and its target proteins, such as fatty acid synthase (FAS) and stearoyl-CoA desaturase (SCD1) in time- and dose-dependent fashions. In contrast, gene expressions of peroxisome proliferator-activated receptor α (PPARα) and CD36 were increased. These effects were reversed in the presence of compound C, an AMPK inhibitor. However, there were no differences in gene expressions of SREBP2, 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, and low-density-lipoprotein receptor (LDLR). Taken together, KRG induced supression of SREBP1c and activation of PPARα via AMPK and these effects seem to be one of anti-hyperlipidemic mechanism of KRG in HepG2 cells.
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KEYWORD
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Korean red ginseng, AMP-activated protein kinase, sterol regulatory element binding protein 1c, peroxisome proliferator-activated receptor α, HepG2 hepatoma cell
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