β-elemene inhibits monocyte–endothelial cells interactions via reactive oxygen species/MAPK/NF-κB signaling pathway in vitro

The recruitment of monocytes to the active endothelial cells is an early step in the formation of atherosclerotic lesions; therefore, the inhibition of monocyte–endothelial cells interactions may serve as a potential therapeutic strategy for atherosclerosis. Recent studies suggest that β-elemene can protect against atherosclerosis in vivo and vitro; however, the mechanism underlying the anti-atherosclerotic effect by β-elemene is not clear yet. In this study, we aimed to investigate the effects of β-elemene on the monocyte–endothelial cells interactions in the initiation of atherosclerosis in vitro. Our results showed that β-elemene protects human umbilical vein endothelial cells (HUVECs) from hydrogen peroxide-induced endothelial cells injury in vitro. Besides, this molecule inhibits monocyte adhesion and transendothelial migration across inflamed endothelium through the suppression of the nuclear factor-kappa B-dependent expression of cell adhesion molecules. Further, β-elemene decreases generation of reactive oxygen species (ROS) and prevents the activation of mitogen-activated protein kinase (MAPK) signaling pathway in HUVECs. In conclusion, this study would provide a new pharmacological evidence of the significance of β-elemene as a future drug for prevention and treatment of atherosclerosis.