Restore the autophagic flux damaged by ox-LDL, and reverse the reduction of LC3II and the accumulation of p62. meanwhile reduces the requirement of ox-LDL and the formation of foam cell by enhancing Sirt1-FOXO1-mediated autophagic flux, indicating the potential of this compound in the therapy of atherosclerosis. This evidence concerns the gene FOXO1 and atherosclerosis.