Cargando…

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...

Descripción completa

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
_version_ 1782413279235145728
author Li, Na
Wang, Ming-Jie
Jin, Sheng
Bai, Ya-Dan
Hou, Cui-Lan
Ma, Fen-Fen
Li, Xing-Hui
Zhu, Yi-Chun
author_facet Li, Na
Wang, Ming-Jie
Jin, Sheng
Bai, Ya-Dan
Hou, Cui-Lan
Ma, Fen-Fen
Li, Xing-Hui
Zhu, Yi-Chun
author_sort Li, Na
collection PubMed
description 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.
format Online
Article
Text
id pubmed-4736414
institution National Center for Biotechnology Information
language English
publishDate 2016
publisher Hindawi Publishing Corporation
record_format MEDLINE/PubMed
spelling pubmed-47364142016-04-07 The H(2)S Donor NaHS Changes the Expression Pattern of H(2)S-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 Oxid Med Cell Longev Research Article 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. Hindawi Publishing Corporation 2016 2016-01-05 /pmc/articles/PMC4736414/ /pubmed/27057284 http://dx.doi.org/10.1155/2016/6492469 Text en Copyright © 2016 Na Li et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Li, Na
Wang, Ming-Jie
Jin, Sheng
Bai, Ya-Dan
Hou, Cui-Lan
Ma, Fen-Fen
Li, Xing-Hui
Zhu, Yi-Chun
The H(2)S Donor NaHS Changes the Expression Pattern of H(2)S-Producing Enzymes after Myocardial Infarction
title The H(2)S Donor NaHS Changes the Expression Pattern of H(2)S-Producing Enzymes after Myocardial Infarction
title_full The H(2)S Donor NaHS Changes the Expression Pattern of H(2)S-Producing Enzymes after Myocardial Infarction
title_fullStr The H(2)S Donor NaHS Changes the Expression Pattern of H(2)S-Producing Enzymes after Myocardial Infarction
title_full_unstemmed The H(2)S Donor NaHS Changes the Expression Pattern of H(2)S-Producing Enzymes after Myocardial Infarction
title_short The H(2)S Donor NaHS Changes the Expression Pattern of H(2)S-Producing Enzymes after Myocardial Infarction
title_sort h(2)s donor nahs changes the expression pattern of h(2)s-producing enzymes after myocardial infarction
topic Research Article
url 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
work_keys_str_mv AT lina theh2sdonornahschangestheexpressionpatternofh2sproducingenzymesaftermyocardialinfarction
AT wangmingjie theh2sdonornahschangestheexpressionpatternofh2sproducingenzymesaftermyocardialinfarction
AT jinsheng theh2sdonornahschangestheexpressionpatternofh2sproducingenzymesaftermyocardialinfarction
AT baiyadan theh2sdonornahschangestheexpressionpatternofh2sproducingenzymesaftermyocardialinfarction
AT houcuilan theh2sdonornahschangestheexpressionpatternofh2sproducingenzymesaftermyocardialinfarction
AT mafenfen theh2sdonornahschangestheexpressionpatternofh2sproducingenzymesaftermyocardialinfarction
AT lixinghui theh2sdonornahschangestheexpressionpatternofh2sproducingenzymesaftermyocardialinfarction
AT zhuyichun theh2sdonornahschangestheexpressionpatternofh2sproducingenzymesaftermyocardialinfarction
AT lina h2sdonornahschangestheexpressionpatternofh2sproducingenzymesaftermyocardialinfarction
AT wangmingjie h2sdonornahschangestheexpressionpatternofh2sproducingenzymesaftermyocardialinfarction
AT jinsheng h2sdonornahschangestheexpressionpatternofh2sproducingenzymesaftermyocardialinfarction
AT baiyadan h2sdonornahschangestheexpressionpatternofh2sproducingenzymesaftermyocardialinfarction
AT houcuilan h2sdonornahschangestheexpressionpatternofh2sproducingenzymesaftermyocardialinfarction
AT mafenfen h2sdonornahschangestheexpressionpatternofh2sproducingenzymesaftermyocardialinfarction
AT lixinghui h2sdonornahschangestheexpressionpatternofh2sproducingenzymesaftermyocardialinfarction
AT zhuyichun h2sdonornahschangestheexpressionpatternofh2sproducingenzymesaftermyocardialinfarction