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- W2013778552 abstract "We previously reported that endogenous H2S contributes to the cardioprotection induced by ischemic preconditioning. In the present study, we further investigated whether extracellular signal regulated kinase (ERK) contributes to the cardioprotection induced by H2S preconditioning (SP). We have examined the effect of NaHS (H2S donor) on myocardial infarction in the isolated rat heart subjected to ischemia insults as well as cell viability, cellular injury index and function in isolated myocytes exposed to simulated ischemia solution. Preconditioning with NaHS for three cycles (3-min each cycle separated by 5-min of recovery) significantly decreased the infarct size in the isolated heart and the cellular injury index in cardiac myocytes whilst increasing cell viability and the amplitude of electrically-induced calcium transients after ischemia/reperfusion in cardiac myocytes. Blockade of ERK with a specific inhibitor, PD98059, significantly attenuated the cardioprotection of SP. Moreover, both SP and ischemic preconditioning (IP) induced phosphorylation of ERK, whereas the activation of ERK by IP was attenuated by inhibition of endogenous H2S with two cystathionine γ-lyase inhibitors, DL-propargylglycine or β-cyano-L-alanine, suggesting that the activation of ERK during IP is, at least partly, mediated by endogenous H2S. In summary, our findings suggest that the cardioprotection of SP is mediated by activation of ERK, by which IP produces the cardioprotection." @default.
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- W2013778552 date "2006-06-01" @default.
- W2013778552 modified "2023-09-27" @default.
- W2013778552 title "A96. Activation of extracellular signal regulated kinase contributes to the cardioprotection by H2S preconditioning" @default.
- W2013778552 doi "https://doi.org/10.1016/j.yjmcc.2006.03.328" @default.
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