Figure 9. Schematic representation of the effects of ES on VbP-treated THP-1 macrophages. VbP exposure induces ROS production, which promotes NLRP3 inflammasome formation leading to activation of caspase-1. Activated caspase-1 triggers pyroptosis through membrane pore formation, DNA fragmentation, and release of mature IL-1β and IL-18. The ensuing sterile inflammatory response contributes in turn to the progression of AS. Meanwhile, ES normalizes Sirt3 expression and promotes autophagy in VbP-treated macrophages. This reduces ROS production and prevents oxidative stress, which inhibits NLRP3 inflammasome formation and prevents pyroptosis.