Nevertheless, silencing of AMPKα and SIRT1 ameliorated colchicine-induced antioxidant enzyme upregulation, lower expression of ROS, downregulation of NLRP3 inflammasome-related proteins, and proinflammatory cytokines, suggesting that the specific mechanism of colchicine inhibiting endothelial cell pyroptosis might be tightly associated with the activation of the AMPK/SIRT1 pathway, which provides a strong theoretical basis for colchicine to become a promising therapeutic drug of atherosclerosis. Here, NLRP3 is linked to atherosclerosis.