Research Paper Volume 12, Issue 2 pp 1704—1724

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

Figure 6. AsC promoted Sirt1 expression in macrophages. 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 AsC (20 μM) for 12 h, and then exposed to ox-LDL for another 24 h. (A) Aortic roots from ApoE−/− mice were stained for the macrophage marker Cd68 and coprobed with antibodies against Sirt1. (B) Quantification of Sirt1 expression in aortic root lesions. (C) Representative photographs of Sirt1 expression, as evaluated by western blot analysis. (D) Statistical results of the Sirt1 expression level compared with that in the control group. (E) Cellular thermal shift assay (CETSA) using macrophage lysates, which were exposed to AsC (20 μM). (F) AsC promoted the resistance of its target protein Sirt1 to proteases (DARTS). (G) Three-dimensional modeling of the binding of AsC to the binding domain of Sirt1. (H) Two-dimensional ligand interaction diagram of AsC and SIRT1. The data are presented as the means ± SDs (n = 5). ##P < 0.01 vs. the control group; *P < 0.05, **P < 0.01 vs. the model group.