Hydrogen sulfide prevents H2O2-induced senescence in human umbilical vein endothelial cells through SIRT1 activation

被引:91
作者
Suo, Rong
Zhao, Zhan-Zhi
Tang, Zhi-Han
Ren, Zhong
Liu, Xing
Liu, Lu-Shan
Wang, Zuo
Tang, Chao-Ke
Wei, Dang-Heng
Jiang, Zhi-Sheng [1 ]
机构
[1] Univ South China, Inst Cardiovasc Dis, Hengyang 421001, Hunan, Peoples R China
基金
高等学校博士学科点专项科研基金; 中国国家自然科学基金;
关键词
sirtuin; 1; oxidative stress; cardiovascular; CARDIOVASCULAR-DISEASE; IN-VITRO; EXPRESSION; INHIBITOR; ARTERIAL; SIGNALS;
D O I
10.3892/mmr.2013.1417
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The aim of the present study was to investigate the attenuation of endothelial cell senescence by H2S and to explore the mechanisms underlying the anti-aging effects of H2S. Senescence was induced in human umbilical vein endothelial cells ( HUVECs) by incubation in 25 mu mol/l H2O2 for 1 h. Senescence-associated beta-galactosidase (SA-beta-gal) activity was examined to determine the effects of H2S on senescent HUVECs. The results indicated that SA-beta-gal activity in the H2O2-treated HUVECs was 11.2 +/- 1.06%, which was attenuated in the NaHS group. Pretreatment with nicotinamide (NAM), a sirtuin 1 (SIRT1) inhibitor, inhibited the reduction in senescence associated with H2S. Immunoblot analyses revealed that SIRT1 levels in senescent HUVECs treated with NaHS (60 mu M) were indistinguishable from controls; however, analyses of SIRT1 activity indicated that SIRT1 enzyme activity was enhanced. In addition, we found that H2S improves the function of senescent HUVECs. The present study demonstrated that H2S protects against HUVEC senescence, potentially through modulation of SIRT1 activity. Furthermore, this study establishes a novel endothelial protective effect of H2S.
引用
收藏
页码:1865 / 1870
页数:6
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