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

Figure 1

Protein levels of PPARδ, p-AMPK, PGC-1α, AT1R, and p-eNOS in HUVECs that were treated with high concentrations of palmitate, cholesterol, and aspirin. The oxygen consumption rate in HUVECs treated with aspirin. (a) (A-1, A-2, A-3, A-4) The protein levels of PPARδ (A-1), p-AMPK (A-2), PGC-1α (A-3), and p-eNOS (A-4) were higher in the CPA group, but they were reversed by a PPARδ antagonist. (A-5) The protein level of AT1R was higher in the CP group, but it was decreased in the CPA group. (b) Aspirin treatment increased the oxygen consumption rate in HUVECs. 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. , , .

(a)

(b)