In this study, we used a FeCl3-induced rat arterial thrombosis model and a human aortic endothelial cell (HAEC) injury model to explore whether ALR-S can inhibit excessive OS and regulate the expression of thrombosis-associated factors through the ERK/NF-κB signaling pathway, leading to antithrombotic effects. The gene discussed is NFKB1; the disease is Arterial thrombosis.