期刊
CELL BIOLOGY INTERNATIONAL
卷 33, 期 10, 页码 1095-1101出版社
WILEY
DOI: 10.1016/j.cellbi.2009.06.029
关键词
Hydrogen sulfide; c-Jun N-terminal kinase; Apoptosis; Ischemia-reperfusion; Cardiomyocyte
类别
资金
- National Natural Science Foundation of China [30700288, 30470688]
- National Basic Research Program of China [2007CB512000]
- Younger Scientists' Foundation of Harbin Medical University [060011]
- Technology Research Foundation of Health Department of Heilongjiang Province [2006-261]
- Postdoctoral Research Foundation of Heilongjiang Province [LRB 07-277]
- Research Foundation of the Health Department of Heilongjiang Province [2005-28]
The mechanism of action of Hydrogen sulfide (H2S) as a novel endogenous gaseous messenger and potential cardioprotectant is not fully understood. We therefore investigated the prevention of cardiomyocyte apoptosis by exogenous H2S and the signaling pathways leading to cardioprotection. Using a simulated ischemia-reperfusion (I/Re) model with primary cultured rat neonatal cardiomyocytes, I/Re induced a rapid, time-dependent phosphorylation of c-Jun N-terminal kinase (JNK), with significant elevation at 0.25 h and a peak at 0.5 h during reperfusion. NaHS (H2S donor) significantly inhibited the early phosphorylation of JNK, especially at 0.5 h. Both NaHS and SP600125 (specific JNK inhibitor) decreased the number of apoptotic cells, lowered cytochrome C release and enhanced Bcl-2 expression. When NaHS application was delayed 1 h after reperfusion, the inhibition of apoptosis by H2S was negated. In conclusion, this is novel evidence that early JNK inhibition during reperfusion is associated with H2S-mediated protection against cardiomyocyte apoptosis. (C) 2009 International Federation for Cell Biology. Published by Elsevier Ltd. All rights reserved.
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