Ginkgolide B suppresses intercellular adhesion molecule-1 expression via blocking nuclear factor-kappaB activation in human vascular endothelial cells stimulated by oxidized low-density lipoprotein.

Abstract

Atherosclerosis is a complex inflammatory arterial disease. Oxidized low-density lipoprotein (ox-LDL) is directly associated with chronic vascular inflammation. In the current study, we tested the hypothesis that ginkgolide B, a component of traditional Chinese herbal medicine for heart disorder, may affect ox-LDL-induced inflammatory responses in human umbilical vein endothelial cells (HUVECs). The results showed that the ox-LDL treatment caused a significantly increase in the expression of intercellular adhesion molecule-1 (ICAM-1) in HUVECs, which was associated with a dramatic augmentation in phosphorylation of IkappaB and relocation of nuclear factor-kappaB (NF-kappaB) into the nuclei. Interestingly, the ox-LDL-induced ICAM-1 expression and NF-kappaB relocation could be attenuated by addition of ginkgolide B. Moreover, ginkgolide B significantly reduces ox-LDL-induced generation of reactive oxygen species (ROS). In conclusion, ginkgolide B may decrease inflammatory responses induced by ox-LDL via blocking NF-kappaB signaling and inhibiting ROS generation in HUVECs.

Cite this paper

@article{Li2009GinkgolideBS, title={Ginkgolide B suppresses intercellular adhesion molecule-1 expression via blocking nuclear factor-kappaB activation in human vascular endothelial cells stimulated by oxidized low-density lipoprotein.}, author={Rui Li and Beidong Chen and Wei Wu and Li Bao and Jian Li and Ruomei Qi}, journal={Journal of pharmacological sciences}, year={2009}, volume={110 3}, pages={362-9} }