The H2S Donor NaHS Changes the Expression Pattern of H2S-Producing Enzymes after Myocardial Infarction
The H2S Donor NaHS Changes the Expression Pattern of H2S-Producing Enzymes after Myocardial Infarction
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H2S 供体 NaHS 改变心肌梗死后 H2S 产生酶的表达模式
DOI：
10.1155/2016/6492469
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发表时间：
2016-01-01
影响因子：
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通讯作者：
Zhu, Yi-Chun
中科院分区：
文献类型：
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作者：
Li, Na;Wang, Ming-Jie;Zhu, Yi-Chun
目标。检测心肌梗死（MI）后NaHS治疗2周后缺血心脏组织中硫化氢（H2S-）生成酶的表达模式和血浆H2S水平，并阐明内源性H2S在MI过程中的作用。结果MI手术后，用H2S供体NaHS治疗2周可减轻缺血性损伤。同时，在缺血心肌中，三种H2S产生酶，即胱硫醚γ-裂解酶（CSE）、胱硫醚-β-合成酶（CBS）和3-巯基丙酮酸硫转移酶（3-MST）均显著增加。血浆H2S水平也升高。在体外，NaHS处理保护心肌细胞免受缺氧损伤，并以浓度依赖性方式提高CBS水平。然而，与体内结果不同，CSE或3-MST表达没有变化。NaHS处理提高了CSE/CBS的活性，但对3-MST的活性无影响。当CSE被敲低（体外）或敲除（体内）时，H2S水平显著降低，随后加剧了缺血性损伤。CBS和3-MST的表达因代偿而增加。结论.外源性H2S处理改变了MI后三种H2S产生酶的表达和H2S水平，表明H2S产生的新的间接调节机制及其对心脏保护的贡献。内源性H2S在MI后保护缺血组织中起重要作用。
Aims. To examine the expression patterns of hydrogen sulphide- (H2S-) producing enzymes in ischaemic heart tissue and plasma levels of H2S after 2 weeks of NaHS treatment after myocardial infarction (MI) and to clarify the role of endogenous H2S in the MI process. Results. After MI surgery, 2 weeks of treatment with the H2S donor NaHS alleviated ischaemic injury. Meanwhile, in ischemia myocardium, three H2S-producing enzymes, cystathionine γ-lyase (CSE), cystathionine-β-synthase (CBS), and 3-mercaptopyruvate sulfurtransferase (3-MST) significantly increased. Plasma H2S levels were also elevated. In vitro, NaHS treatment protected cardiomyocytes from hypoxic injury and raised CBS levels in a concentration-dependent manner. Different from in vivo results, however, CSE or 3-MST expression did not change. NaHS treatment increased the activity of CSE/CBS but not of 3-MST. When CSE was either knocked down (in vitro) or knocked out (in vivo), H2S levels significantly decreased, which subsequently exacerbated the ischaemic injury. Meanwhile, the expressions of CBS and 3-MST increased due to compensation. Conclusions. Exogenous H2S treatment changed the expressions of three H2S-producing enzymes and H2S levels after MI, suggesting a new and indirect regulatory mechanism for H2S production and its contribution to cardiac protection. Endogenous H2S plays an important role in protecting ischaemic tissue after MI.