Korean Red Ginseng Attenuates Hepatic Lipid Accumulation via AMPK Activation in Human Hepatoma Cells

• Published in: Food science and biotechnology 2010, 19(1), , pp.207-212
• Main Authors: Quan, Hai-Yan, Kyung Hee University, Seoul, Republic of Korea, Yuan, Hai-Dan, Kyung Hee University, Seoul, Republic of Korea, Kim, D.Y., Kyung Hee University, Seoul, Republic of Korea, Zhang, Ya, Kyung Hee University, Seoul, Republic of Korea, Chung, S.H., Kyung Hee University, Seoul, Republic of Korea
• Format: Article
• Language: English
• Subjects: AMP-activated protein kinase; Chemistry; Chemistry and Materials Science; Food Science; HepG2 hepatoma cell; Korean red ginseng; Nutrition; PANAX PSEUDOGINSENG; peroxisome proliferator-activated receptor alpha; Research Article; sterol regulatory element binding protein 1c; 식품과학
• ISSN: 1226-7708; 2092-6456
• DOI: 10.1007/s10068-010-0028-8

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.