In the current study, we investigated the delayed cardioprotection induced by H(2)S preconditioning in an in vivo rat model of myocardial infarction. Assessment of infarct size revealed that a single bolus of NaHS (a donor of H(2)S, at 0.1-10 micromol/kg body weight) administered 1 day before myocardial infarction produced a strong infarct-limiting effect. A time course study demonstrated that the protection lasted at least 3 days after the preconditioning stimulus. We further compared the effect of H(2)S preconditioning with post-infarction treatment. Although injection of NaHS (1 micromol/kg once daily) for 3 days after myocardial infarction also significantly decreased infarct size, the protective effect was significantly lower than that afforded by H(2)S preconditioning. A combination of both preconditioning and post-treatment did not produce a stronger protection compared with H(2)S preconditioning alone. Pretreatment with chelerythrine chloride (5 mg/kg, i.p.), a protein kinase C (PKC) inhibitor, 15 min before NaHS administration blocked the infarct-sparing effect of H(2)S preconditioning. In conclusion, the current study provided the first evidence that H(2)S preconditioning produces strong late cardioprotection through a PKC-dependent mechanism. Such protection could not be reproduced by H(2)S treatment after the infarction occurred. A combination of both preconditioning and post-treatment does not provide additional benefit and hence is not necessary when the access to preconditioning has been secured.
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http://dx.doi.org/10.1016/j.ejphar.2009.05.023 | DOI Listing |
Free Radic Biol Med
November 2024
Department of Physiology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, PR China. Electronic address:
Proc Natl Acad Sci U S A
March 2024
Department of Biological Chemistry, University of Michigan Medical Center, Ann Arbor, MI 48109-0600.
Hydrogen sulfide exposure in moderate doses can induce profound but reversible hypometabolism in mammals. At a cellular level, HS inhibits the electron transport chain (ETC), augments aerobic glycolysis, and glutamine-dependent carbon utilization via reductive carboxylation; however, the durability of these changes is unknown. We report that despite its volatility, HS preconditioning increases , the O pressure for half-maximal cellular respiration, and has pleiotropic effects on oxidative metabolism that persist up to 24 to 48 h later.
View Article and Find Full Text PDFWorld J Stem Cells
February 2024
Basic Sciences, Sulaiman AlRajhi University, Albukairiyah 52736, AlQaseem, Saudi Arabia.
In this editorial, we comment on the article published in the recent issue of the . They focus on stem cell preconditioning to prevent ferroptosis by modulating the cystathionine γ-lyase/hydrogen sulfide (HS) pathway as a novel approach to treat vascular disorders, particularly pulmonary hypertension. Preconditioned stem cells are gaining popularity in regenerative medicine due to their unique ability to survive by resisting the harsh, unfavorable microenvironment of the injured tissue.
View Article and Find Full Text PDFHydrogen sulfide exposure in moderate doses can induce profound but reversible hypometabolism in mammals. At a cellular level, H S inhibits the electron transport chain (ETC), augments aerobic glycolysis, and glutamine-dependent carbon utilization via reductive carboxylation; however, the durability of these changes is unknown. We report that despite its volatility, H S preconditioning increases , the O pressure for half maximal cellular respiration, and has pleiotropic effects on oxidative metabolism that persist up to 24-48 h later.
View Article and Find Full Text PDFPurpose: Remote ischemic preconditioning (RIPC) confers cardioprotection against ischemia reperfusion (IR) injury. However, the precise mechanisms involved in RIPC-induced cardioprotection are not fully explored. The present study was aimed to identify the role of melatonin in RIPC-induced late cardioprotective effects in rats and to explore the role of H2S, TNF-α and mitoKATP in melatonin-mediated effects in RIPC.
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