Catalpol Attenuates Hepatic Steatosis by Regulating Lipid Metabolism via AMP-Activated Protein Kinase Activation

Figure 3

AMPK activation mediates catalpol-regulated lipid metabolism in palmitate- (PA-) treated HepG2 cells. HepG2 cells were treated with PA (300 μM) and/or catalpol (400 μM) for 24 h. Compound C (10 μM) was added 2 h prior to the cotreatment with PA and catalpol. (a) Protein expressions of p-AMP-activated protein kinase (AMPK), p-acetyl-CoA carboxylase (ACC), precursor and mature sterol regulatory element-binding protein 1c (preSREBP-1c and mSREBP-1c, respectively), fatty acid synthase (FAS), peroxisome proliferator-activated receptor α (PPARα), and carnitine palmitoyltransferase 1 (CPT1) were analyzed via Western blotting. (b–d) Densitometric analyses of the band intensity ratios of p-AMPK/AMPK, p-ACC/ACC, preSREBP-1c, mSREBP-1c, FAS, PPARα, and CPT1. Data are presented as the of three independent experiments. vs. the Normal group; ^#, ^## vs. the catalpol group.

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