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

Figure 4

CCR2 western blot analysis and immunocytochemistry of mannose receptor in RAW 264.7 cells treated with high concentrations of palmitate, cholesterol, and aspirin. (a) The protein level of CCR2 was lower in the CPA group than that of the CP group; however, the effect of aspirin was reversed by treatment with a PPARδ antagonist. (b) The protein expression of mannose receptor was increased by aspirin treatment. But the effect of aspirin was offset by 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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