Aspirin Improves Nonalcoholic Fatty Liver Disease and Atherosclerosis through Regulation of the PPARδ-AMPK-PGC-1α Pathway in Dyslipidemic Conditions

Figure 2

Protein levels of PPARδ, p-AMPK, PGC-1α, FAS, HMGCR, NF-κB, and AT1R in HepG2 cells that were treated with high concentrations of palmitate, cholesterol, and aspirin. The oxygen consumption rate in HepG2 cells treated with aspirin. The effects of AMPK antagonist on p-AMPK and PPARδ protein levels in HepG2 cells. (a) (A-1, A-2, A-3) The protein levels of PPARδ (A-1), p-AMPK (A-2), and PGC-1α (A-3) were higher in the CPA group than those of the CP group; however, the effects of aspirin were reversed by treatment with a PPARδ antagonist. (A-4, A-5, A-6, A-7) The protein levels of FAS (A-4), HMGCR (A-5), NF-κB (A-6), and AT1R (A-7) were lower in the CPA group than those of the CP group; however, the effects of aspirin were reversed by treatment with a PPARδ antagonist. (b) The oxygen consumption rate was increased by aspirin treatment. (c) AMPK antagonist, Compound C, decreased only the protein expression of p-AMPK. The results are expressed as (). Values were statistically analyzed by unpaired -test and one-way ANOVA. An upper line on the three bars means one-way ANOVA analysis. All experiments were repeated three and over times. Meaning of indications: Ctrl is an untreated control group, CP is a cholesterol and palmitate-treated group, CPA is a cholesterol, palmitate, and aspirin-treated group, and CPAG is a cholesterol, palmitate, aspirin, and GSK0660-treated group. , , .

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