Resveratrol protects human endothelium from H2O2-induced oxidative stress and senescence via SirT1 activation

Chung Lan Kao, Liang Kung Chen, Yuh Lih Chang, Ming Chih Yung, Chuan Chih Hsu, Yu Chih Chen, Wen Liang Lo, Shih Jen Chen, Hung Hai Ku, Shin Jang Hwang

Research output: Contribution to journalArticle

150 Citations (Scopus)

Abstract

Aim: Silencing information regulator (SirT1), a NAD-dependent histone deacetylase, is an essential media- tor of longevity in normal cells by calorie restriction. SirT1 has many biological functions, including tran- scription regulation, cell differentiation inhibition, cell cycle regulation, and anti-apoptosis. Resveratrol (RV)- induced SirT1 activation also improves endothelial dysfunction and suppresses vascular inflammation. In this study, we investigated the roles of RV-induced SirT1 activation in endothelial cells under oxidative stress. Methods: SirT1 mRNA expression levels were examined in the endothelium layer (endothelial cells) of cardi- ac coronary vessels from patients receiving coronary artery bypass graft surgery (CABG) surgery and aged rats using reverse transcriptase polymerase chain reaction (RT-PCR). To further explore the effect of SirT1 activa- tion on oxidative stress-induced aging, senescence-associated β-galactosidase (SA-β-gal) expression in RV- treated human umbilical vein endothelial cells (HUVECs) with or without H2O2 treatment was evaluated. Results: SirT1 expression was decreased in aged and atherosclerotic vessels in vivo, and significantly reduced in endothelial cells purified from vessel tissues. Furthermore, SirT1 levels were dose-depend- ently increased in RV-treated HUVECs. The SA-β gal assay showed that RV inhibited the senescent phenotype of H2O2-treated HUVECs. Reactive oxygen species (ROS) production and the percentage of cells positive for SA-β gal were significantly increased in siRNA-SirT1 (knockdown of SirT1 expression)-treated HUVEC cells. Importantly, the treatment effect of RV was significantly abolished in the oxidative effects of H2O2-treated HUVECs by siRNA-SirT1. Conclusion: Our data suggested that SirT1 could be a crucial factor involved in the endothelial cells of atherosclerotic CAGB patients and aging rats. RV is a potential candidate for preventing oxidative stress-induced aging in endothelial cells. RV may also prevent ROS-induced damage via increased endothelial SirT1 expression.

Original languageEnglish
Pages (from-to)970-979
Number of pages10
JournalJournal of Atherosclerosis and Thrombosis
Volume17
Issue number9
Publication statusPublished - 2010
Externally publishedYes

Fingerprint

Oxidative stress
Endothelial cells
Endothelium
Oxidative Stress
Chemical activation
Human Umbilical Vein Endothelial Cells
Endothelial Cells
Small Interfering RNA
Aging of materials
Reactive Oxygen Species
Surgery
Galactosidases
Rats
Histone Deacetylases
resveratrol
Reverse Transcriptase Polymerase Chain Reaction
Coronary Artery Bypass
NAD
Polymerase chain reaction
RNA-Directed DNA Polymerase

Keywords

  • Cardiovascular dysfunction
  • Human umbilical vein endothelial cells
  • NAD-dependent histone deacetylase
  • Resveratrol
  • SirT1

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Internal Medicine
  • Biochemistry, medical

Cite this

Kao, C. L., Chen, L. K., Chang, Y. L., Yung, M. C., Hsu, C. C., Chen, Y. C., ... Hwang, S. J. (2010). Resveratrol protects human endothelium from H2O2-induced oxidative stress and senescence via SirT1 activation. Journal of Atherosclerosis and Thrombosis, 17(9), 970-979.

Resveratrol protects human endothelium from H2O2-induced oxidative stress and senescence via SirT1 activation. / Kao, Chung Lan; Chen, Liang Kung; Chang, Yuh Lih; Yung, Ming Chih; Hsu, Chuan Chih; Chen, Yu Chih; Lo, Wen Liang; Chen, Shih Jen; Ku, Hung Hai; Hwang, Shin Jang.

In: Journal of Atherosclerosis and Thrombosis, Vol. 17, No. 9, 2010, p. 970-979.

Research output: Contribution to journalArticle

Kao, CL, Chen, LK, Chang, YL, Yung, MC, Hsu, CC, Chen, YC, Lo, WL, Chen, SJ, Ku, HH & Hwang, SJ 2010, 'Resveratrol protects human endothelium from H2O2-induced oxidative stress and senescence via SirT1 activation', Journal of Atherosclerosis and Thrombosis, vol. 17, no. 9, pp. 970-979.
Kao, Chung Lan ; Chen, Liang Kung ; Chang, Yuh Lih ; Yung, Ming Chih ; Hsu, Chuan Chih ; Chen, Yu Chih ; Lo, Wen Liang ; Chen, Shih Jen ; Ku, Hung Hai ; Hwang, Shin Jang. / Resveratrol protects human endothelium from H2O2-induced oxidative stress and senescence via SirT1 activation. In: Journal of Atherosclerosis and Thrombosis. 2010 ; Vol. 17, No. 9. pp. 970-979.
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abstract = "Aim: Silencing information regulator (SirT1), a NAD-dependent histone deacetylase, is an essential media- tor of longevity in normal cells by calorie restriction. SirT1 has many biological functions, including tran- scription regulation, cell differentiation inhibition, cell cycle regulation, and anti-apoptosis. Resveratrol (RV)- induced SirT1 activation also improves endothelial dysfunction and suppresses vascular inflammation. In this study, we investigated the roles of RV-induced SirT1 activation in endothelial cells under oxidative stress. Methods: SirT1 mRNA expression levels were examined in the endothelium layer (endothelial cells) of cardi- ac coronary vessels from patients receiving coronary artery bypass graft surgery (CABG) surgery and aged rats using reverse transcriptase polymerase chain reaction (RT-PCR). To further explore the effect of SirT1 activa- tion on oxidative stress-induced aging, senescence-associated β-galactosidase (SA-β-gal) expression in RV- treated human umbilical vein endothelial cells (HUVECs) with or without H2O2 treatment was evaluated. Results: SirT1 expression was decreased in aged and atherosclerotic vessels in vivo, and significantly reduced in endothelial cells purified from vessel tissues. Furthermore, SirT1 levels were dose-depend- ently increased in RV-treated HUVECs. The SA-β gal assay showed that RV inhibited the senescent phenotype of H2O2-treated HUVECs. Reactive oxygen species (ROS) production and the percentage of cells positive for SA-β gal were significantly increased in siRNA-SirT1 (knockdown of SirT1 expression)-treated HUVEC cells. Importantly, the treatment effect of RV was significantly abolished in the oxidative effects of H2O2-treated HUVECs by siRNA-SirT1. Conclusion: Our data suggested that SirT1 could be a crucial factor involved in the endothelial cells of atherosclerotic CAGB patients and aging rats. RV is a potential candidate for preventing oxidative stress-induced aging in endothelial cells. RV may also prevent ROS-induced damage via increased endothelial SirT1 expression.",
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T1 - Resveratrol protects human endothelium from H2O2-induced oxidative stress and senescence via SirT1 activation

AU - Kao, Chung Lan

AU - Chen, Liang Kung

AU - Chang, Yuh Lih

AU - Yung, Ming Chih

AU - Hsu, Chuan Chih

AU - Chen, Yu Chih

AU - Lo, Wen Liang

AU - Chen, Shih Jen

AU - Ku, Hung Hai

AU - Hwang, Shin Jang

PY - 2010

Y1 - 2010

N2 - Aim: Silencing information regulator (SirT1), a NAD-dependent histone deacetylase, is an essential media- tor of longevity in normal cells by calorie restriction. SirT1 has many biological functions, including tran- scription regulation, cell differentiation inhibition, cell cycle regulation, and anti-apoptosis. Resveratrol (RV)- induced SirT1 activation also improves endothelial dysfunction and suppresses vascular inflammation. In this study, we investigated the roles of RV-induced SirT1 activation in endothelial cells under oxidative stress. Methods: SirT1 mRNA expression levels were examined in the endothelium layer (endothelial cells) of cardi- ac coronary vessels from patients receiving coronary artery bypass graft surgery (CABG) surgery and aged rats using reverse transcriptase polymerase chain reaction (RT-PCR). To further explore the effect of SirT1 activa- tion on oxidative stress-induced aging, senescence-associated β-galactosidase (SA-β-gal) expression in RV- treated human umbilical vein endothelial cells (HUVECs) with or without H2O2 treatment was evaluated. Results: SirT1 expression was decreased in aged and atherosclerotic vessels in vivo, and significantly reduced in endothelial cells purified from vessel tissues. Furthermore, SirT1 levels were dose-depend- ently increased in RV-treated HUVECs. The SA-β gal assay showed that RV inhibited the senescent phenotype of H2O2-treated HUVECs. Reactive oxygen species (ROS) production and the percentage of cells positive for SA-β gal were significantly increased in siRNA-SirT1 (knockdown of SirT1 expression)-treated HUVEC cells. Importantly, the treatment effect of RV was significantly abolished in the oxidative effects of H2O2-treated HUVECs by siRNA-SirT1. Conclusion: Our data suggested that SirT1 could be a crucial factor involved in the endothelial cells of atherosclerotic CAGB patients and aging rats. RV is a potential candidate for preventing oxidative stress-induced aging in endothelial cells. RV may also prevent ROS-induced damage via increased endothelial SirT1 expression.

AB - Aim: Silencing information regulator (SirT1), a NAD-dependent histone deacetylase, is an essential media- tor of longevity in normal cells by calorie restriction. SirT1 has many biological functions, including tran- scription regulation, cell differentiation inhibition, cell cycle regulation, and anti-apoptosis. Resveratrol (RV)- induced SirT1 activation also improves endothelial dysfunction and suppresses vascular inflammation. In this study, we investigated the roles of RV-induced SirT1 activation in endothelial cells under oxidative stress. Methods: SirT1 mRNA expression levels were examined in the endothelium layer (endothelial cells) of cardi- ac coronary vessels from patients receiving coronary artery bypass graft surgery (CABG) surgery and aged rats using reverse transcriptase polymerase chain reaction (RT-PCR). To further explore the effect of SirT1 activa- tion on oxidative stress-induced aging, senescence-associated β-galactosidase (SA-β-gal) expression in RV- treated human umbilical vein endothelial cells (HUVECs) with or without H2O2 treatment was evaluated. Results: SirT1 expression was decreased in aged and atherosclerotic vessels in vivo, and significantly reduced in endothelial cells purified from vessel tissues. Furthermore, SirT1 levels were dose-depend- ently increased in RV-treated HUVECs. The SA-β gal assay showed that RV inhibited the senescent phenotype of H2O2-treated HUVECs. Reactive oxygen species (ROS) production and the percentage of cells positive for SA-β gal were significantly increased in siRNA-SirT1 (knockdown of SirT1 expression)-treated HUVEC cells. Importantly, the treatment effect of RV was significantly abolished in the oxidative effects of H2O2-treated HUVECs by siRNA-SirT1. Conclusion: Our data suggested that SirT1 could be a crucial factor involved in the endothelial cells of atherosclerotic CAGB patients and aging rats. RV is a potential candidate for preventing oxidative stress-induced aging in endothelial cells. RV may also prevent ROS-induced damage via increased endothelial SirT1 expression.

KW - Cardiovascular dysfunction

KW - Human umbilical vein endothelial cells

KW - NAD-dependent histone deacetylase

KW - Resveratrol

KW - SirT1

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