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Anti-apoptotic action of hydrogen sulfide is associated with early JNK inhibition

Authors

  • Sa Shi,

    Corresponding author
    1. Department of Pathophysiology, Harbin Medical University, Harbin 150081, China
      E-mail addresses: shisa1976@hotmail.com
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    • These authors contributed equally to this work.

  • Qing-song Li,

    1. Department of Cardiology, the Second Affiliated Hospital of Harbin Medical University, Harbin 150086, PR China
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    • These authors contributed equally to this work.

  • Hong Li,

    1. Department of Pathophysiology, Harbin Medical University, Harbin 150081, China
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  • Li Zhang,

    1. Department of Pathophysiology, Harbin Medical University, Harbin 150081, China
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  • Man Xu,

    1. Department of Pathophysiology, Harbin Medical University, Harbin 150081, China
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  • Jia-li Cheng,

    1. Department of Cardiology, the Second Affiliated Hospital of Harbin Medical University, Harbin 150086, PR China
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  • Cheng-hai Peng,

    1. Department of Cardiology, the Second Affiliated Hospital of Harbin Medical University, Harbin 150086, PR China
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  • Chang-qing Xu,

    1. Department of Pathophysiology, Harbin Medical University, Harbin 150081, China
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  • Ye Tian

    Corresponding author
    1. Department of Pathophysiology, Harbin Medical University, Harbin 150081, China
    2. Department of Cardiology, the Second Affiliated Hospital of Harbin Medical University, Harbin 150086, PR China
      Department of Pathophysiology, Harbin Medical University, Harbin 150081, China. Tel./fax: +86 451 86674548 E-mail addresses: tianye@ems.hrbmu.edu.cn
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Department of Pathophysiology, Harbin Medical University, Harbin 150081, China. Tel./fax: +86 451 86674548 E-mail addresses: tianye@ems.hrbmu.edu.cn

E-mail addresses: shisa1976@hotmail.com

Abstract

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.

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