Figure 5. Autophagy inhibition abolished AsC-mediated antiatherosclerotic effects and macrophage polarization. All mice were fed a HFD in the presence or absence of AsC (20 mg·kg-1·day-1, i.g.) for 4 weeks. In the in vitro assay, RAW264.7 cells were pretreated with 3-MA (5 mM) for 2 h, treated with AsC (20 μM) for 12 h, and then exposed to ox-LDL for another 24 h. (A) Representative images of oil red O staining of the aortic root. (B) Quantification of the total plaque area. (C) Dual immunofluorescence staining forArg1 (red) and DAPI (blue) in lesions in the aortic root. (D) Representative images of oil red O staining of ox-LDL-treated RAW264.7 cells. (E) The percentage of plaque area relative to lumen area. (F) Quantification of relative fluorescence intensity. (G) Quantification of oil red O staining, as detected by a microplate reader. (H) Representative photographs of Arg1, Mrc1, Cd86 and BECN1 expression, as evaluated by western blot analysis. (I) Statistical results of Mrc1, Cd86 and Arg1 expression levels compared with those in the ox-LDL-treated group. The data are presented as the means ± SDs (n = 5). *P < 0.05, **P < 0.01 vs. the model group; $P < 0.05, $$P < 0.01 vs. the ox-LDL and AsC group.