Liraglutide Attenuates Nonalcoholic Fatty Liver Disease through Adjusting Lipid Metabolism via SHP1/AMPK Signaling Pathway
Figure 5
AMPK inhibitor could block liraglutide induced reduction of lipid lipogenesis and without change on SHP1 expression. (a) HepG2 cells were cultured in FBS-free DMEM and then subjected to 250 nmol/L PA in 24 hours and exposed to indicated drugs for 4 hours. And cells were stained with Oil Red O and photographed under the microscope (magnification ×200, scale 20 μm). (b) Intracellular lipid accumulation was quantified by semiquantitative analysis. The rate of cell with positive area is shown as mean ± SD of three independent experiments. (c, d) Effect of AMPK inhibitor compound C (CC) on protein expression of SHP1, p-AMPK, AMPK, p-ACC, and ACC in vitro. The densitometry ratio of SHP1/GAPDH, p-AMPK/AMPK, and p-ACC/ACC are shown as mean ± SD of three independent experiments. (e, f) Effect of CC on protein expression of lipogenesis proteins (FAS and SREBP-1c) in vitro. The densitometry ratio of FAS/GAPDH and SREBP-1c/GAPDH is shown as mean ± SD of three independent experiments. Whole-cell protein was harvest and detected by western blot. The representative images are shown. The western blot results were normalized to the CTL group value. denotes P < 0.05 versus the CTL group. # denotes P < 0.05 versus the LR group.