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DOI 10.1155/2016/6492469

Медицинская библиотека · Oxidative medicine and cellular longevity · 2016

The H2S Donor NaHS Changes the Expression Pattern of H2S-Producing Enzymes after Myocardial Infarction.

Li Na, Wang Ming-Jie, Jin Sheng, Bai Ya-Dan, Hou Cui-Lan, Ma Fen-Fen, Li Xing-Hui, Zhu Yi-Chun

СтатьяПоддержка исследования: вне правительства СШАПеревод в очереди

Аннотация

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.

Для цитирования: Li Na, Wang Ming-Jie, Jin Sheng, Bai Ya-Dan, Hou Cui-Lan, Ma Fen-Fen, Li Xing-Hui, Zhu Yi-Chun. The H2S Donor NaHS Changes the Expression Pattern of H2S-Producing Enzymes after Myocardial Infarction.. Oxidative medicine and cellular longevity. 2016. DOI: 10.1155/2016/6492469.

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