Ginkgolide C alleviates atherosclerosis via activating Nrf2 to inhibit ROS‑dependent NLRP3 inflammasome activation

(oxidized‑low density lipoprotein‑stimulated aortic endothelial cells) models were established. Comprehensive analyses included histopathological characterization, lipid profiling, ultrastructural examination, redox‑inflammatory biomarker quantification, and molecular pathway validation. GC significantly attenuated hyperlipidemia and plaque progression while preserving vascular ultrastructure. Mechanistically, GC enhanced endothelial survival through dual pathway modulation: i) Nrf2 nuclear translocation upregulated antioxidant enzymes [heme oxygenase‑1/NAD(P)H quinone oxidoreductase 1/glutamate‑cysteine ligase modifier subunit], restoring redox homeostasis; ii) NLRP3 inflammasome inhibition via Caspase‑1 suppression mitigated inflammatory cytokine release. The present study demonstrated GC's dual‑target therapeutic efficacy against AS through Nrf2‑mediated oxidative stress resolution and NLRP3 inflammasome inactivation, offering new insights into phytochemical‑based cardiovascular interventions.