Ginsenoside Rg1 activates AMPK to inhibit lipid deposition in a cell model of non-alcoholic fatty liver disease

Abstract

Objective To investigate the effect of ginsenoside Rg1 on lipid deposition in a cell model of non-alcoholic fatty liver disease (NAFLD) and explore the molecular mechanism. Methods HepG2 cells were treated with 0.25 mmol/L palmitic acid for 24 h to induce changes mimicking NAFLD, followed by treatment with 40 μg/mL ginsenoside Rg1 or 5 μmol/L metformin for 6 h with or without pretreatment with 10 μmol/L Compound C (CC, an AMPK inhibitor) for 1 h. The level of triglyceride (TG) in the cells was detected using a micromethod, and the accumulation of lipid droplets was observed using Oil Red O staining. RT-qPCR and Western blotting were employed to detect the alterations in the mRNA and protein expression of the key genes related to the AMPK pathway. Results Compared with the control cells, the cell model of NAFLD showed significantly increased intracellular TG level and lipid droplet accumulation (P < 0.05), which were both reduced obviously after Rg1 treatment (P < 0.05). Rg1 significantly abolished palmitic acid-induced inhibition of phosphorylation of intracellular AMPK and acetyl-CoA carboxylase (ACC), and down-regulated the expression of sterol regulatory element-binding protein-1c and fatty acid synthase (P < 0.05). Pretreatment with CC significantly antagonized the effects of Rg1 on intracellular TG, lipid deposition and AMPK pathway in palmitic acid-induced cells (P < 0.05). Conclusion Ginsenoside Rg1 can ameliorate lipid deposition in the cell model of NAFLD by activating the AMPK pathway.

Keywords

• non-alcoholic fatty liver disease
• ginsenoside rg1
• lipid deposition
• amp-activated protein kinase