Fig. 9

Schematic representation of the effects of MT on nicotine-treated THP-1 macrophages. Nicotine exposure induces ROS production, which promotes NLRP3 inflammasome formation, leading to the activation of caspase-1. Activated caspase-1 triggers pyroptosis through membrane pore formation, DNA fragmentation, and the release of mature IL-1β and IL-18. The ensuing sterile inflammation contributes to the progression of AS. Moreover, MT normalizes Sirt3 expression and promotes FOXO3α expression in nicotine-treated macrophages. This reduces ROS production and prevents oxidative stress, which inhibits NLRP3 inflammasome formation and prevents pyroptosis. The process by which MT inhibits nicotine-induced pyroptosis also involves apoptosis, which is mainly due to the interaction between caspase-1 and caspase-3. ↑ induce; ⊥ inhibit