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|標題:||Ginkgo biloba extract attenuates oxLDL-induced oxidative functional damages in endothelial cells||作者:||Ou, H.C.
|關鍵字:||endothelium;adhesion molecule;apoptosis;reactive oxygen species;low-density-lipoprotein;monocyte chemoattractant protein-1;laser-scanning cytometry;nitric-oxide;induced apoptosis;oxidized ldl;cardiovascular-diseases;leukocyte adhesion;nadph oxidase;double-blind||Project:||Journal of Applied Physiology||期刊/報告no：:||Journal of Applied Physiology, Volume 106, Issue 5, Page(s) 1674-1685.||摘要:||
Ou HC, Lee WJ, Lee IT, Chiu TH, Tsai KL, Lin CY, Sheu WH. Ginkgo biloba extract attenuates oxLDL-induced oxidative functional damages in endothelial cells. J Appl Physiol 106: 1674-1685, 2009. First published February 19, 2009; doi:10.1152/japplphysiol.91415.2008.-Atherosclerosis is a chronic inflammatory process with increased oxidative stress in vascular endothelium. Ginkgo biloba extract (GbE), extracted from Ginkgo biloba leaves, has commonly been used as a therapeutic agent for cardiovascular and neurological disorders. The aim of this study was to investigate how GbE protects vascular endothelial cells against the proatherosclerotic stressor oxidized low-density lipoprotein (oxLDL) in vitro. Human umbilical vein endothelial cells (HUVECs) were incubated with GbE (12.5-100 mu g/ml) for 2 h and then incubated with oxLDL (150 mu g/ml) for an additional 24 h. Subsequently, reactive oxygen species (ROS) generation, antioxidant enzyme activities, adhesion to monocytes, cell morphology, viability, and several apoptotic indexes were assessed. Our data show that ROS generation is an upstream signal in oxLDL-treated HUVECs. Cu,Zn-SOD, but not Mn-SOD, was inactivated by oxLDL. In addition, oxLDL diminished expression of endothelial NO synthase and enhanced expression of adhesion molecules (ICAM, VCAM, and E-selectin) and the adherence of monocytic THP-1 cells to HUVECs. Furthermore, oxLDL increased intracellular calcium, disturbed the balance of Bcl-2 family proteins, destabilized mitochondrial membrane potential, and triggered subsequent cytochrome c release into the cytosol and activation of caspase-3. These detrimental effects were ameliorated dose dependently by GbE (P < 0.05). Results from this study may provide insight into a possible molecular mechanism underlying GbE suppression of the oxLDL-mediated vascular endothelial dysfunction.
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