Ginkgolide B Suppresses Intercellular Adhesion Molecule-1 Expression via Blocking Nuclear Factor-κB 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 d...

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Bibliographic Details
Main Authors: Rui Li, Beidong Chen, Wei Wu, Li Bao, Jian Li, Ruomei Qi
Format: Article
Language:English
Published: Elsevier 2009-01-01
Series:Journal of Pharmacological Sciences
Online Access:http://www.sciencedirect.com/science/article/pii/S1347861319311855
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Summary: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 IκB and relocation of nuclear factor-κB (NF-κB) into the nuclei. Interestingly, the ox-LDL–induced ICAM-1 expression and NF-κB 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-κB signaling and inhibiting ROS generation in HUVECs. Keywords:: ginkgolide B, intercellular adhesion molecule-1 (ICAM-1), oxidized low-density lipoprotein (LDL), nuclear factor-κB (NF-κB), endothelial cell
ISSN:1347-8613