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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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. ©2009 The Japanese Pharmacological Society.

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Li, R., Chen, B., Wu, W., Bao, L., Li, J., & Qi, R. (2009). 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, 110(3), 362–369. https://doi.org/10.1254/jphs.08275FP

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