FIGURE 6.

AICAR increases ABCG1 expression and inhibits atherogenesis in apoE^−/− mice. ApoE^−/− mice, fed a high fat cholesterol diet, were randomly administered with either AICAR (n = 8, 200 mg·kg⁻¹·day⁻¹) or vehicle (n = 8, 0.9% NaCl) for 12 weeks. A, peritoneal macrophages were isolated, lysed, and subjected to Western blot to evaluate the protein levels of ABCG1 and β-actin. B, quantification of ABCG1 protein relative levels. **, p < 0.01. C and D, peritoneal macrophages from vehicle- and AICAR-treated mice were preincubated with compound C or transfected with ABCG1 siRNA for 6 h, followed by the treatment of OxLDL (50 μg/ml) for an additional 24 h. After incubation, cells were fixed and stained with Oil Red O to detect lipid accumulation. Hematoxylin was used as counterstaining. **, p < 0.01. E, determination of atherosclerotic lesion size in apoE^−/− mice. The aortic roots of the animals treated as described were analyzed for atherosclerotic lesion size with Oil Red O staining. Magnification was ×400. F, quantitative analysis of the atherosclerotic lesion areas in the aortic sinus (n = 8, **, p < 0.01).