J Pharmacol Sci. 2009 Jul ;110(3):362-9. PMID: 19609067
Ginkgolide B suppresses intercellular adhesion molecule-1 expression by way of blocking nuclear factor-kappaB activation in human vascular endothelial cells stimulated by oxidized low-density lipoprotein.
Atherosclerosis is a posh inflammatory arterial illness. Oxidized low-density lipoprotein (ox-LDL) is instantly related to persistent vascular irritation. Within the present research, we examined the speculation that ginkgolide B, a part of conventional Chinese language natural drugs for coronary heart dysfunction, might have an effect on ox-LDL-induced inflammatory responses in human umbilical vein endothelial cells (HUVECs). The outcomes confirmed that the ox-LDL remedy precipitated a considerably improve within the expression of intercellular adhesion molecule-1 (ICAM-1) in HUVECs, which was related to a dramatic augmentation in phosphorylation of IkappaB and relocation of nuclear factor-kappaB (NF-kappaB) into the nuclei. Apparently, the ox-LDL-induced ICAM-1 expression and NF-kappaB relocation could possibly be attenuated by addition of ginkgolide B. Furthermore, ginkgolide B considerably reduces ox-LDL-induced era of reactive oxygen species (ROS). In conclusion, ginkgolide B might lower inflammatory responses induced by ox-LDL by way of blocking NF-kappaB signaling and inhibiting ROS era in HUVECs.