Acteoside and 6-O-Acetylacteoside Downregulate Cell Adhesion Molecules Induced by IL-1 beta through Inhibition of ERK and JNK in Human Vascular Endothelial Cells

Abstract

Acteoside, an active phenylethanoid glycoside of many medicinal plants and bitter tea, displays anti-inflammatory 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-1 beta-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-1 beta-activated HUVECs. The inhibition of acteoside and 6-O-acetylacteoside on IL-1 beta-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.