Resveratrol Protects Human Endothelium from H2O2-Induced Oxidative Stress and Senescence via SirT1 Activation

DOI PubMed 被引用文献6件 参考文献43件
  • Kao Chung-Lan
    Department of Physical Medicine and Rehabilitation, Taipei Veterans General Hospital. Center for Geriatrics and Gerontology, Taipei Veterans General Hospital. School of Medicine, National Yang-Ming University.
  • Chen Liang-Kung
    Department of Family Medicine, Taipei Veterans General Hospital. Center for Geriatrics and Gerontology, Taipei Veterans General Hospital. School of Medicine, National Yang-Ming University.
  • Chang Yuh-Lih
    Department of Medical Research and Education, Taipei Veterans General Hospital & National Yang-Ming University. Institute of Anatomy and Cell Biology, Institute of Pharmacology, National Yang-Ming University.
  • Yung Ming-Chih
    Department of Cardiovascular Surgery, Taiwan Adventist Hospital. School of Medicine, National Yang-Ming University.
  • Hsu Chuan-Chih
    Department of Surgery, Chi-Mei Medical Center & Chia Nan University of Pharmacy & Science.
  • Chen Yu-Chih
    Department of Medical Research and Education, Taipei Veterans General Hospital & National Yang-Ming University. School of Medicine, National Yang-Ming University.
  • Lo Wen-Liang
    Institute of Anatomy and Cell Biology, Institute of Pharmacology, National Yang-Ming University. School of Medicine, National Yang-Ming University.
  • Chen Shih-Jen
    Department of Medical Research and Education, Taipei Veterans General Hospital & National Yang-Ming University. School of Medicine, National Yang-Ming University.
  • Ku Hung-Hai
    Institute of Anatomy and Cell Biology, Institute of Pharmacology, National Yang-Ming University.
  • Hwang Shin-Jang
    Department of Family Medicine, Taipei Veterans General Hospital. Center for Geriatrics and Gerontology, Taipei Veterans General Hospital. School of Medicine, National Yang-Ming University.

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Aim: Silencing information regulator (SirT1), a NAD-dependent histone deacetylase, is an essential mediator of longevity in normal cells by calorie restriction. SirT1 has many biological functions, including transcription 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.<BR>Methods: SirT1 mRNA expression levels were examined in the endothelium layer (endothelial cells) of cardiac 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 activation 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.<BR>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-dependently 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.<BR>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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