CXCR4 was involved in andrographolide inhibits atherosclerosis by inactivating the PI3K/AKT/NF-κB signaling pathway

Atherosclerosis is one of the major diseases that seriously impacts human health, which has been conceived as a complex process. In this study, we sought to explore the role and the underlying mechanism of Andrographolide (Andro) in Atherosclerosis progress. The CCK8 and flow cytometry were respectively used to explore the effect of Andro on cell proliferation and apoptosis. Then, we detected the effect of Andro on inflammatory factors. Next, the connection of Andro and CXCR4 and the underlying mechanism was researched. Our study proved that Andro could promotes cell proliferation and inhibits cell apoptosis. And, Andro significantly inhibits the expression of TNF-alpha, IL-6, endothelian 1 (ET-1), MMP-9 and malondialdehyde (MDA). Further, we have also confirmed that CXCR4 was involved in the Andro regulation progress in atherosclerosis inhibition by inactivating the PI3K/AKT/NF-kappa B signaling pathway. All these findings suggest that Andro inhibits atherosclerosis and may be involved in progression of atherosclerosis and could be a new therapeutic target for this disease.