Fig. 7.

IMB17–15 alleviated OA-induced steatosis and TG accumulation by stimulating the AMPK pathway and upregulating PPARα expression in HL-7702 cells. Cells were left untreated or treated with OA and different concentrations of IMB17–15, as indicated, for 24 h. a Cell total proteins were extracted. P-AMPKα, AMPKα, p-ACC and ACC protein expression levels were determined by western blotting and were normalized against β-actin protein expression levels. b IMB17–15 enhanced the mRNA expression of PPARα and its downstream lipid oxidation- and lipoprotein metabolism-related genes, includingPPARA, CPT1A, SCP-2, ApoA-I and ApoA-V, in a dose-dependent manner. ACTB served as the loading control. After treatment, the cells were also subjected to ORO staining (c) and harvested for intracellular TG assay (d) to investigate the influence of IMB17–15 on lipid metabolism (magnification ×400). ACC acetyl-CoA carboxylase, AMPKα adenosine monophosphate (AMP)-activated protein kinase, ApoA-I apolipoprotein A-I, ApoA-V Apolipoprotein A-V, CPT1A carnitine palmitoyltransferase I, OA oleic acid, PPARα peroxisome proliferator activated receptor α, SCP-2 sterol carrier protein 2. The values are expressed as the mean ± SD of five independent assays, ^#P < 0.05 versus the control group, ^##P < 0.01 versus the control group, **P < 0.01 versus the OA-induced group, ^ΔΔP < 0.01; indicates that the control group was significantly different from the OA-induced group; ANOVA followed by Duncan's multiple range tests