Protective Effects of Hydrogen Sulfide Against Chronic Alcohol Intake-Induced Left Ventricular Remodeling in Rats
Protective Effects of Hydrogen Sulfide Against Chronic Alcohol Intake-Induced Left Ventricular Remodeling in Rats
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DOI：
10.1007/s10557-013-6441-5
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发表时间：
2013-01
影响因子：
3.4
通讯作者：
Xiaoping Zhou;Xiang Lu;Wei-ting Xu;Jianchang Chen
中科院分区：
文献类型：
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作者：
Xiaoping Zhou;Xiang Lu;Wei-ting Xu;Jianchang Chen
目的探讨硫化氢（H2S）对慢性酒精摄入所致左室重构的保护作用及其机制。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左室重构。通过检测培养上清液中MDA、GSH-Px、Tot-SOD、CuZn-SOD和Mn-SOD的含量来评价氧化应激。Annexin V/PI双染流式细胞仪检测心肌细胞凋亡率。Western blotting检测Bcl-2家族凋亡调节蛋白的表达。结果超声心动图和形态计量学数据表明，硫化氢对慢性酒精摄入引起的左室重构具有保护作用。结果表明，与对照组相比，酒精组MDA含量显著升高，GSH-Px、Tot-SOD、CuZn-SOD和Mn-SOD活性显著降低;与酒精组相比，酒精+ NaHS组MDA含量显著降低，GSH-Px、Tot-SOD、CuZn-SOD和Mn-SOD活性显著升高。酒精组细胞凋亡率显著高于对照组，而酒精+ NaHS组细胞凋亡率显著低于酒精组。此外，Bcl-2和Bcl-xL的表达上调和Bax的表达下调，在酒精+ NaHS组相比，酒精group.ConclusionsOur研究表明，硫化氢保护慢性酒精摄入诱导的左心室重构通过衰减氧化应激和细胞凋亡。
PurposeTo investigate the protective effects of hydrogen sulfide (H2S) against chronic alcohol intake-induced left ventricular remodeling and explore the potential mechanisms involved.MethodsRats 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.ResultsThe echocardiographic and morphometric data indicated that H2S 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.ConclusionsOur study demonstrates that H2S protects against chronic alcohol intake-induced left ventricular remodeling via attenuating oxidative stress and apoptosis.