Research Paper Volume 12, Issue 2 pp 1704—1724

Araloside C attenuates atherosclerosis by modulating macrophage polarization via Sirt1-mediated autophagy

Figure 7. AsC-induced autophagy and M2 phenotype polarization were Sirt1-dependent in ox-LDL-treated macrophages. Sirt1 was inhibited by 10 μM EX527 for 6 h or knocked down by siRNA, as described in the Materials and Methods section. Twenty-four hours posttransfection, cells were treated with AsC (20 μM) for 12 h and then incubated with ox-LDL (80 μg/mL) for an additional 24 h. (A, C) Representative immunofluorescence images showing Mrc1 and ATG5 expression in RAW264.7 cells. (B, D) The relative quantitative analysis of Mrc1 and ATG5 fluorescence in RAW264.7 cells. (E) Representative western blot analysis of Mrc1, Arg1, Cd86, BECN1, ATG5, LC3, Sirt1 and β-actin in macrophages. (F) Quantification of the expression of Mrc1, Arg1, Cd86, BECN1, ATG5, LC3, and Sirt1. The data are presented as the means ± SDs (n = 5). *P < 0.05, **P < 0.01 vs. the ox-LDL group; $P < 0.05, $$P < 0.01 vs. the ox-LDL and AsC group.