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The H(2)S Donor NaHS Changes the Expression Pattern of H(2)S-Producing Enzymes after Myocardial Infarction

Aims. To examine the expression patterns of hydrogen sulphide- (H(2)S-) producing enzymes in ischaemic heart tissue and plasma levels of H(2)S after 2 weeks of NaHS treatment after myocardial infarction (MI) and to clarify the role of endogenous H(2)S in the MI process. Results. After MI surgery, 2...

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Detalles Bibliográficos
Autores principales: Li, Na, Wang, Ming-Jie, Jin, Sheng, Bai, Ya-Dan, Hou, Cui-Lan, Ma, Fen-Fen, Li, Xing-Hui, Zhu, Yi-Chun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4736414/
https://www.ncbi.nlm.nih.gov/pubmed/27057284
http://dx.doi.org/10.1155/2016/6492469
Descripción
Sumario:Aims. To examine the expression patterns of hydrogen sulphide- (H(2)S-) producing enzymes in ischaemic heart tissue and plasma levels of H(2)S after 2 weeks of NaHS treatment after myocardial infarction (MI) and to clarify the role of endogenous H(2)S in the MI process. Results. After MI surgery, 2 weeks of treatment with the H(2)S donor NaHS alleviated ischaemic injury. Meanwhile, in ischemia myocardium, three H(2)S-producing enzymes, cystathionine γ-lyase (CSE), cystathionine-β-synthase (CBS), and 3-mercaptopyruvate sulfurtransferase (3-MST) significantly increased. Plasma H(2)S 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), H(2)S levels significantly decreased, which subsequently exacerbated the ischaemic injury. Meanwhile, the expressions of CBS and 3-MST increased due to compensation. Conclusions. Exogenous H(2)S treatment changed the expressions of three H(2)S-producing enzymes and H(2)S levels after MI, suggesting a new and indirect regulatory mechanism for H(2)S production and its contribution to cardiac protection. Endogenous H(2)S plays an important role in protecting ischaemic tissue after MI.