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Ginkgo biloba extract attenuates oxLDL-induced oxidative functional damages in endothelial cells

¹Department of Physical Therapy, College of Health Care, China Medical University, Taichung; ²Department of Education and Medical Research, Taichung Veterans General Hospital, Taichung; ³Department of Obstetrics and Gynecology, China Medical University Hospital, Taichung; ⁴Graduate Institute of Clinical Medical Science, China Medical University, Taichung; ⁵Department of Biotechnology, China Medical University, Taichung; ⁶Division of Endocrinology and Metabolism, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung; ⁷Institute of Medical Technology, National Chung-Hsing University, Taichung; ⁸Chung Shan Medical University, Taichung; and ⁹College of Medicine, National Yang-Ming University, Taipei, Taiwan

Submitted 24 October 2008 ; accepted in final form 18 February 2009

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 µg/ml) for 2 h and then incubated with oxLDL (150 µg/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.

endothelium; adhesion molecule; apoptosis; reactive oxygen species