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

Figure 3

Immunocytochemistry for TNFα and Oil Red O staining in HepG2 cells treated with high concentrations of palmitate, cholesterol, and aspirin. (a) The elevated TNFα protein expression in the CP group was decreased by aspirin; however, the effect of aspirin was reversed by treatment with a PPARδ antagonist. (b) Lipid accumulation increased in the CP group was decreased by aspirin treatment; however, the effect of aspirin was offset by treatment with a PPARδ antagonist. Images were taken at ×200 magnification. 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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