Ginkgo biloba extract attenuates oxLDL-induced oxidative functional damages in endothelial cells. Journal of Appylied Physiology

中國醫藥大學機構典藏 China Medical University Repository, Taiwan > 健康照護學院 > 物理治療學系(停用) > 期刊論文 > Item 310903500/1626

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题名:	Ginkgo biloba extract attenuates oxLDL-induced oxidative functional damages in endothelial cells. Journal of Appylied Physiology
作者:	歐秀中(Hsiu-Chung Ou);李文珍(Lee WJ);李奕德(Lee IT);邱燦宏(Tsan-Hung Chiu);蔡昆霖(Tsai KL);林芷穎(Lin CY);許惠恒(Sheu WH)*
贡献者:	健康照護學院物理治療學系
日期:	2009-05
上传时间:	2009-08-19 17:04:10 (UTC+8)
摘要:	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 microg/ml) for 2 h and then incubated with oxLDL (150 microg/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.
關聯:	JOURNAL OF APPLIED PHYSIOLOGY106(5):1674~1685
显示于类别:	[物理治療學系(停用)] 期刊論文

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