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
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
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DOI:
10.1254/jphs.08275fp
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发表时间:
2009-07-01
影响因子:
3.5
通讯作者:
Qi, Ruomei
中科院分区:
文献类型:
--
作者:
Li, Rui;Chen, Beidong;Qi, Ruomei
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 I kappa B and relocation of nuclear factor-kappa B (NF-kappa B) into the nuclei. Interestingly, the ox-LDL-induced ICAM-1 expression and NF-kappa B 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-kappa B signaling and inhibiting ROS generation in HUVECs.