Artemisinin Inhibits Monocyte Adhesion To Huvecs Through The Nf-B And Mapk Pathways In Vitro

The adhesion of monocytes to human umbilical vein endothelial cells (HUVECs) plays a crucial role in the initiation of atherosclerosis. Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are two important molecules involved in the adhesion of monocytes to HUVECs. Previous studies have suggested that artemisinin, apart from an anti-malarial agent, also has other effects. In the present study, we found that artemisinin significantly decreased the adhesion of monocytes to tumor necrosis factor- (TNF-)-stimulated HUVECs in a dose-dependent manner and suppressed the mRNA and protein level of ICAM-1 and VCAM-1 in the TNF--stimulated HUVECs. In addition, the nuclear factor-B (NF-B) inhibitor, Bay 11-7082, and mitogen-activated protein kinase (MAPK) inhibitors (SB203580 and U0126) respectively reduced the adhesion of monocytes to TNF--stimulated HUVECs, and suppressed ICAM-1 and VCAM-1 expression in TNF- stimulated HUVECs. Moreover, artemisinin impeded the activation of the NF-B and MAPK signaling pathways. Furthermore, Bay 11-7082 significantly decreased the phosphorylation of levels extracellular signal-regulated protein kinase (ERK)1/2, p38 and c-Jun N-terminal kinase (JNK). Taken together, the findings of our study indicated that artemisinin blocked monocyte adhesion to TNF--stimulated to HUVECs by downregulating ICAM-1 and VCAM-1 expression in the TNF--stimulated HUVECs. Artemisinin may thus have potential for use in the protection against the early development of atherosclerotic lesions.