首页> 美国卫生研究院文献>Cell Bioscience >Exogenous H2S contributes to recovery of ischemic post-conditioning-induced cardioprotection by decrease of ROS level via down-regulation of NF-κB and JAK2-STAT3 pathways in the aging cardiomyocytes
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Exogenous H2S contributes to recovery of ischemic post-conditioning-induced cardioprotection by decrease of ROS level via down-regulation of NF-κB and JAK2-STAT3 pathways in the aging cardiomyocytes

机译:外源性H2S通过下调衰老心肌细胞中NF-κB和JAK2-STAT3途径的ROS水平来降低缺血后调节诱导的心脏保护作用

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摘要

BackgroundHydrogen sulfide (H2S), a third member of gasotransmitter family along with nitric oxide and carbon monoxide, generated from mainly catalyzed by cystathionine-lyase, possesses important functions in the cardiovascular system. Ischemic post-conditioning (PC) strongly protects against the hypoxia/reoxygenation (H/R)-induced injury and apoptosis of cardiomyocytes. However, PC protection is ineffective in the aging cardiomyocytes. Whether H2S restores PC-induced cardioprotection by decrease of reactive oxygen species (ROS) level in the aging cardiomyocytes is unknown.
机译:背景技术硫化氢(H2S)是一类气体递质家族的第三个成员,与一氧化氮和一氧化碳一起主要由胱硫醚裂解酶催化产生,在心血管系统中具有重要的功能。缺血后处理(PC)可以有效防止缺氧/复氧(H / R)引起的心肌细胞损伤和凋亡。但是,PC保护在衰老的心肌细胞中无效。 H2S是否通过减少老化心肌细胞中的活性氧(ROS)水平来恢复PC诱导的心脏保护作用尚不清楚。

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