Emodin reduces FFAs-induced fatty degeneration in HepG2 cells via the AMPK/SREBP-1 pathway / 中国医师杂志

ABSTRACT

Objective To investigate the effects of emodin on the triglyceride metabolism and oxidative stress in steatosis in HepG2 cells and possible underlying mechanisms.Methods The appropriate concentration of emodin on HepG2 cells were detected by methyl thiazolyl tetrazolium (MTT) assay.HepG2 cells were induced to fat overaccumulation by 1 mmol/L free fatty acids (FFA) (oleate∶ palmitate =2∶1).The model group exposed to 10 μmol/L,20 μmol/L,40 μmol/L emodin.The intracellular lipid accumulation was documented by Oil Red O staining and the content of triglyceride and total cholesterol was observed.Reactive oxygen species (ROS) was determined by flow cytometry.Western blotting was performed to analyze the protein levels of adenosine monophosphate-activated protein kinase (AMPK),phosphorylated AMPK,and sterol regulatory element-binding protein 1 (SREBP-1).Results Emodin reduced lipid accumulation and triglycerides (TG) content (P ＜ 0.05).At the same time,it significantly reduced ROS production (P ＜ 0.05).Moreover,the levels of AMPK and p-AMPK protein were significantly upregulated,and SREBP-1 protein was significantly downregulated with the treatment of emodin (P ＜ 0.01).Conclusions This study has demonstrated that emodin can reduce fatty degeneration induced by FFAs in hepatocytes,and this effect may be partially mediated by the AMPK/SREBP-1 pathway.