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硫化氢对慢性酒精摄入诱导大鼠左心室重构的保护作用。

Protective effects of hydrogen sulfide against chronic alcohol intake-induced left ventricular remodeling in rats.

机构信息

Department of Cardiology, The Second Affiliated Hospital of Soochow University, No.1055 Sanxiang Road, Suzhou 215004, China.

出版信息

Cardiovasc Drugs Ther. 2013 Jun;27(3):221-7. doi: 10.1007/s10557-013-6441-5.

DOI:10.1007/s10557-013-6441-5
PMID:23344930
Abstract

PURPOSE

To investigate the protective effects of hydrogen sulfide (H(2)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 H(2)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 H(2)S protects against chronic alcohol intake-induced left ventricular remodeling via attenuating oxidative stress and apoptosis.

摘要

目的

研究硫化氢(H₂S)对慢性酒精摄入诱导的左心室重构的保护作用,并探讨其潜在机制。

方法

将大鼠随机分为 4 组:酒精组、NaHS 组、酒精+NaHS 组和对照组。通过超声心动图和形态计量学研究评估左心室重构。通过检测上清液中的 MDA、GSH-Px、总 SOD、CuZn-SOD 和 Mn-SOD 来评估氧化应激。通过 Annexin V/PI 染色流式细胞术测定心肌细胞凋亡率。通过 Western 印迹检测凋亡调节蛋白 Bcl-2 家族的表达。

结果

超声心动图和形态计量学数据表明,H₂S 对慢性酒精摄入诱导的左心室重构具有保护作用。与对照组相比,酒精组 MDA 水平显著升高,GSH-Px、总 SOD、CuZn-SOD 和 Mn-SOD 活性显著降低;而在酒精+NaHS 组,MDA 水平显著降低,GSH-Px、总 SOD、CuZn-SOD 和 Mn-SOD 活性显著升高。与对照组相比,酒精组的细胞凋亡率显著升高,而酒精+NaHS 组的细胞凋亡率显著降低。此外,与酒精组相比,酒精+NaHS 组的 Bcl-2 和 Bcl-xL 表达上调,Bax 表达下调。

结论

本研究表明,H₂S 通过减轻氧化应激和凋亡来保护慢性酒精摄入诱导的左心室重构。

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