Protective Effects of Hydrogen Sulfide Against Chronic Alcohol Intake-Induced Left Ventricular Remodeling in Rats

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• 作者：Xiang Zhou (1)
  Xiang Lu (2)
  Weiting Xu (1)
  Jianchang Chen (1)
  
• 关键词：Hydrogen sulfide ; Alcohol ; Left ventricular remodeling ; Oxidative stress ; Apoptosis
• 刊名：Cardiovascular Drugs and Therapy
• 出版年：2013
• 出版时间：June 2013
• 年：2013
• 卷：27
• 期：3
• 页码：221-227
• 全文大小：325KB
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• 作者单位：Xiang Zhou (1)
  Xiang Lu (2)
  Weiting Xu (1)
  Jianchang Chen (1)
  
  1. Department of Cardiology, The Second Affiliated Hospital of Soochow University, No.1055 Sanxiang Road, Suzhou, 215004, China
  2. Department of Geriatrics, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China
  
• ISSN：1573-7241

文摘

Purpose To investigate the protective effects of hydrogen sulfide (H2sub>S) against chronic alcohol intake-induced left ventricular remodeling and explore the potential mechanisms involved. Methods Rats were randomly divided into 4 groups: alcohol group, NaHS group, alcohol + NaHS group, and control group. The echocardiographic and morphometric studies were performed to assess left ventricular remodeling. Oxidative stress was evaluated by detecting MDA, GSH-Px, Tot-SOD, CuZn-SOD and Mn-SOD in the supernatant. Cardiomyocyte apoptotic rate was determined by flow cytometry with Annexin V/PI staining. Western blotting was conducted to detect the expression of Bcl-2 family of apoptosis regulator proteins. Results The echocardiographic and morphometric data indicated that H2sub>S has protective effects against chronic alcohol intake-induced left ventricular remodeling. Our findings showed a significant increase in MDA level and decreases in GSH-Px, Tot-SOD, CuZn-SOD and Mn-SOD activities in the alcohol group compared to the control group, while in the alcohol + NaHS group, a significant decrease in MDA level and increases in GSH-Px, Tot-SOD, CuZn-SOD and Mn-SOD activities were found compared to the alcohol group. The apoptotic rate in the alcohol group was significantly higher than in the control group, whereas apoptotic rate in the alcohol + NaHS group was significantly lower than in the alcohol group. In addition, Bcl-2 and Bcl-xL expression was upregulated and Bax expression was downregulated in the alcohol + NaHS group compared to the alcohol group. Conclusions Our study demonstrates that H2sub>S protects against chronic alcohol intake-induced left ventricular remodeling via attenuating oxidative stress and apoptosis.