Acteoside and 6-o-acetylacteoside downregulate cell adhesion molecules induced by IL-1beta; through inhibition of ERK and JNK in human vascular endothelial cells

Acteoside, an aclive phenylethanoid glycoside of many medicinal plants and bitter tea, displays antiinflammatory properties in vitro. However, it is unclear whether acteoside and similar compounds may inhibit the expression of cell adhesion molecules (CAMs), which plays a role in the pathogenesis of atherosclerosis and inflammation. Here, we found that acteoside, isoacteoside, and 6-O-acetylacteoside inhibited IL-1β-activated expression of intercellular CAM-1 (ICAM-1) and vascular CAM-1 (VCAM-1) in human umbilical vein endothelial cells (HUVECs); the inhibitory potency was as follows: 6-O-acetylacteoside > acteoside > isoacteoside. Acteoside and 6-O-acetylacteoside also dose-dependently inhibited VCAM-1 gene promoter activity in IL-1β-activated HUVECs. The inhibition of acteoside and 6-O-acetylacteoside on IL-1β-activated expression of CAMs was manifested by decreased phosphorylation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK). These results indicate that acteoside and 6-O-acetylacteoside may exert anti-inflammatory activities in vascular endothelium by inhibiting the expression of CAMs, primarily through decreased phosphorylation of ERK and JNK.