Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function
Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function
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DOI：
10.1073/pnas.0705891104
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发表时间：
2007-09-25
影响因子：
11.1
通讯作者：
Lefer, David J.
中科院分区：
文献类型：
--
作者：
Elrod, John W.;Calvert, John W.;Lefer, David J.
最近发现硫化氢（H2S）是一种内源性产生的气体第二信使，能够调节许多生理过程，就像一氧化氮一样，促使我们研究H2S作为心脏保护剂的潜力。在目前的研究中，我们证明了在心肌缺血再灌注（MI-R）的体内模型中，在再灌注时递送H2S限制了梗死面积并保留了左心室（LV）功能。这种观察到的细胞保护作用与抑制心肌炎症和保护I-R损伤后的线粒体结构和功能有关。此外，我们表明，调制内源性产生的硫化氢的心脏特异性过表达的胱硫醚γ-裂解酶（α-MHC-CGL-Tg小鼠）显着限制损伤的程度。这些研究结果表明，H2S可能是在心肌梗死的演变过程中的细胞保护的价值，无论是管理H2S或内源性生产的调制可能是缺血性疾病的临床受益。
The recent discovery that hydrogen sulfide (H2S) is an endogenously produced gaseous second messenger capable of modulating many physiological processes, much like nitric oxide, prompted us to investigate the potential of H2S as a cardioprotective agent. In the current study, we demonstrate that the delivery of H2S at the time of reperfusion limits infarct size and preserves left ventricular (LV) function in an in vivo model of myocardial ischemia reperfusion (MI-R). This observed cytoprotection is associated with an inhibition of myocardial inflammation and a preservation of both mitochondrial structure and function after I-R injury. Additionally, we show that modulation of endogenously produced H2S by cardiac-specific overexpression of cystathionine gamma-lyase (alpha-MHC-CGL-Tg mouse) significantly limits the extent of injury. These findings demonstrate that H2S may be of value in cytoprotection during the evolution of myocardial infarction and that either administration of H2S or the modulation of endogenous production may be of clinical benefit in ischemic disorders.