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遗传和药理学硫化治疗减轻了小鼠缺血引起的心力衰竭
John W Calvert1, Marah Elston, Chad K Nicholson
1Department of Surgery, Emory University School of Medicine, Atlanta, GA 30308, USA.
Circulation
|June 23, 2010
概括
硫化 (H(2) S) 对心力衰竭具有治疗潜力. 固体H2S生产和外部H2S治疗都能保护心脏免受缺血引起的损伤,并提高存活率.
科学领域:
- 心血管研究研究心血管研究
- 分子医学是分子医学.
- 生物化学 生物化学
背景情况:
- 硫化 (H2S) 是一种具有已知的细胞保护性质的内源信号分子.
- 在心力衰竭模型中H(2) S的治疗潜力需要进一步研究.
研究的目的:
- 在心力衰竭的小鼠模型中评估H(2) S的治疗疗效.
- 在心肌缺血的背景下研究H(2) S的保护机制.
主要方法:
- 在小鼠中,通过永久冠状动脉绑定或缺血-再输液诱导心力衰竭.
- 心脏特异性cystathionine gamma-lyase (alphaMHC-CGL-Tg(+)) 的过度表达被用来调节内源的H(2) S.
- 外源的H(2) S疗法 (Na(2) S) 在缺血后进行.
主要成果:
- 过度表达H(2) S生成酶的转基因小鼠显示出对左心室功能障碍的保护,并改善了生存率.
- 外源H(2) S疗法减轻了结构和功能恶化,氧化应激和线粒体功能障碍.
- H(2) S疗法增加了Akt酸化和Nrf2和NRF1的核转移,增强了抗氧化防御和线粒体生物发生.
结论:
- 调节内源H2S的产生或给予外源H2S可能为缺血引起的心力衰竭提供治疗效益.
- H(2) S通过多个分子通路表现出显著的心脏保护作用.
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