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

Journal of Pharmacological Sciences

Jian Li¹  Beidong Chen¹  Wei Wu¹  Rui Li¹  Li Bao¹  Ruomei Qi¹ 

[1] Beijing Institute of Geriatrics, Beijing Hospital and Key Laboratory of Geriatrics Ministry of Health, China

关键词: ginkgolide B;    intercellular adhesion molecule-1 (ICAM-1);    oxidized low-density lipoprotein (LDL);    nuclear factor-κB (NF-κB);    endothelial cell;   

DOI  :  10.1254/jphs.08275FP

学科分类：药学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(38)Cited-By(11)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.

【 授权许可】

Unknown