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

Hsiu Chung Ou, Wen Jane Lee, I. Te Lee, Tsan Hung Chiu, Kun Ling Tsai, Chih Ying Lin, Wayne Huey Herng Sheu

Research output: Contribution to journalArticle

53 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)1674-1685
Number of pages12
JournalJournal of Applied Physiology
Volume106
Issue number5
DOIs
Publication statusPublished - 2009 May 1

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

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