کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8345236 | 1541613 | 2015 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Hydrogen sulfide protects against apoptosis under oxidative stress through SIRT1 pathway in H9c2 cardiomyocytes
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کلمات کلیدی
Sirt1H2SSirtuin-1ROS - ROSHydrogen peroxide - آب اکسیژنهOxidative stress - تنش اکسیداتیوHydrogen sulfide - سولفید هیدروژنSodium hydrogen sulfide - سولفید هیدروژن سدیمMitochondrial function - عملکرد میتوکندریheart failure - نارسایی قلبیNash - نوشNitric oxide - نیتریک اکسیدH2O2 - هیدروژن پراکسیدReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Oxidative stress plays a great role in the pathogenesis of heart failure (HF). Oxidative stress results in apoptosis, which can cause the damage of cardiomyocytes. Hydrogen sulfide (H2S), the third gasotransmitter, is a good reactive oxygen species (ROS) scavenger, which has protective effect against HF. Sirtuin-1 (SIRT1) is a highly conserved nicotinamide adenine dinucleotide (NAD)-dependent histone deacetylase that plays a critical role in promoting cell survival under oxidative stress. The purpose of this article is to investigate the interaction between H2S and SIRT1 under oxidative stress in H9c2 cardiomyocytes. Oxidative stress was induced by hydrogen peroxide (H2O2). Treatment with NaSH (25-100âµmol/L) dose-dependently increased the cell viability and improved the cell apoptosis induced by H2O2 in H9c2 cardiomyocytes. The protective effect of NaSH against the apoptosis could be attenuated by SIRT1 inhibitor Ex 527 (10âµmol/L). Treatment with NaSH (100âµmol/L) could increase the expression of SIRT1 in time dependent manner, which decreased by different concentration of H2O2. NaSH (100âµmol/L) increased the cellular ATP level and the expression of ATPase. These effects were attenuated by Ex 527 (10âµmol/L). After NaSH (100âµmol/L) treatment, the decrease in ROS production and the enhancement in SOD, GPx and GST expression were observed. Ex 527 (10âµmol/L) reversed these effects. In conclusion, for the first time, this article can identify antioxidative effects of H2S under oxidative stress through SIRT1 pathway in H9c2 cardiomyocytes.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Nitric Oxide - Volume 46, 30 April 2015, Pages 204-212
Journal: Nitric Oxide - Volume 46, 30 April 2015, Pages 204-212
نویسندگان
Dan Wu, Qingxun Hu, Xinhua Liu, Lilong Pan, Qinghui Xiong, Yi Zhun Zhu,