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

研究成果: Article

51 引文 (Scopus)

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 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.

原文English
頁(從 - 到)1674-1685
頁數12
期刊Journal of Applied Physiology
106
發行號5
DOIs
出版狀態Published - 2009 五月 1

指紋

Ginkgo biloba
Endothelial Cells
Human Umbilical Vein Endothelial Cells
Reactive Oxygen Species
Cardiovascular Agents
E-Selectin
Mitochondrial Membrane Potential
Vascular Endothelium
Cytochromes c
oxidized low density lipoprotein
Nervous System Diseases
Nitric Oxide Synthase
Caspase 3
Cytosol
Superoxide Dismutase
Blood Vessels
Monocytes
Cell Survival
Atherosclerosis
Oxidative Stress

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

引用此文

Ou, Hsiu Chung ; Lee, Wen Jane ; Lee, I. Te ; Chiu, Tsan Hung ; Tsai, Kun Ling ; Lin, Chih Ying ; Sheu, Wayne Huey Herng. / Ginkgo biloba extract attenuates oxLDL-induced oxidative functional damages in endothelial cells. 於: Journal of Applied Physiology. 2009 ; 卷 106, 編號 5. 頁 1674-1685.
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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.",
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Ginkgo biloba extract attenuates oxLDL-induced oxidative functional damages in endothelial cells. / Ou, Hsiu Chung; Lee, Wen Jane; Lee, I. Te; Chiu, Tsan Hung; Tsai, Kun Ling; Lin, Chih Ying; Sheu, Wayne Huey Herng.

於: Journal of Applied Physiology, 卷 106, 編號 5, 01.05.2009, p. 1674-1685.

研究成果: Article

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AU - Lee, Wen Jane

AU - Lee, I. Te

AU - Chiu, Tsan Hung

AU - Tsai, Kun Ling

AU - Lin, Chih Ying

AU - Sheu, Wayne Huey Herng

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AB - 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.

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