Protective role of betulinic acid on TNF-alpha-induced cell adhesion molecules in vascular endothelial cells.

Vascular inflammation is an important event in the development of vascular diseases such as tumor progression and atherosclerosis. In the present study, betulinic acid (BA) treatment was found to show potent inhibitory effect on vascular inflammation process by TNF-alpha in human umbilical vein endothelial cells (HUVEC). Pretreatment of HUVEC with BA was blocked TNF-alpha induced expression level of cell adhesion molecules such as intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), endothelial cell selectin (E-selectin) as well as gelatinase in TNF-alpha-activated HUVEC in a dose-dependent manner. When preincubated with BA, the adhesion of HL-60 cells to TNF-alpha-induced HUVEC was significantly decreased in a concentration-dependent manner. TNF-alpha-induced intracellular ROS was markedly decreased by pretreatment with BA. Furthermore, BA significantly inhibited the translocation and transcriptional activity of NF-kappaB increased by TNF-alpha. In conclusion, these results suggested a vascular protective role of BA via inhibition of ROS and NF-kappaB activation in HUVEC. Copyright 2009 Elsevier Inc. All rights reserved.