Research Paper Volume 12, Issue 2 pp 1704—1724

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

Figure 4. AsC induced macrophage autophagy. 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 photographs of autophagosomes (red arrows) examined using a JEOL JEM1230 electron microscope. (B) Statistical results of autophagosomes. (C) Summarized data showing the percentage of cells that were positive for CytoID fluorescence, as detected by flow cytometry analysis. (D) Representative photographs of LC3II staining. (E) Statistical results of LC3II-positive cells. (F) Representative photographs of ATG5, BECN1, P62, LC3 and β-actin expression in ox-LDL-treated macrophages, as evaluated by western blot analysis. (G) Statistical results of ATG5, BECN1, P62, LC3II/LC3I expression levels compared with those in the control group. (H) Representative photographs of BECN1, P62, LC3 and β-actin expression in aortic lysates. (I) Statistical results of BECN1, P62, LC3II/LC3I expression levels compared to those in the control group. The data are presented as the means ± SDs (n = 5). #P < 0.05, ##P < 0.01 vs. the control group, *P < 0.05, **P < 0.01 vs. the model group; $P < 0.05 vs. the ox-LDL and AsC group.