{"title":"Hemin as a protective agent in an in vitro model of hypoxia/reoxygenation-induced injury.","authors":"Zuoyan Wang, Wei Liu","doi":"10.1177/20503121251329163","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Ischemia-reperfusion injury exacerbates myocardial damage and affects the prognosis of patients with ST-elevation myocardial infarction. This study investigates the potential cytoprotective effects of hemin in an in vitro cardiomyocyte model subjected to hypoxia/reoxygenation, a simulation of ischemia-reperfusion injury, building upon previous evidence of hemin's efficacy in modulating ischemia-reperfusion injuries in various biological tissues.</p><p><strong>Methods: </strong>H9c2 cardiomyocytes were exposed to a simulated hypoxia/reoxygenation environment. The experimental setup included pretreatment with hemin at varying concentrations, with subsequent assessment in the presence and absence of a heme oxygenase-1 inhibitor (Zinc-Protoporphyrin IX (heme oxygenase-1 inhibitor)).</p><p><strong>Results: </strong>Pretreatment with 5 μM hemin notably attenuated the oxidative stress and apoptosis in H9c2 cardiomyocytes following hypoxia/reoxygenation exposure, while simultaneously upregulating heme oxygenase-1 expression. This protective effect was found to be heme oxygenase-1 dependent, as evidenced by its attenuation upon the introduction of Zinc-Protoporphyrin IX (heme oxygenase-1 inhibitor), a heme oxygenase-1 inhibitor.</p><p><strong>Conclusion: </strong>The findings suggest that low-dose, short-term hemin pretreatment can effectively reduce hypoxia/reoxygenation-induced cellular damage in cardiomyocytes through the upregulation of heme oxygenase-1. These results underscore the therapeutic potential of hemin in attenuating myocardial hypoxia/reoxygenation injury.</p>","PeriodicalId":21398,"journal":{"name":"SAGE Open Medicine","volume":"13 ","pages":"20503121251329163"},"PeriodicalIF":2.3000,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11938892/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"SAGE Open Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1177/20503121251329163","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: Ischemia-reperfusion injury exacerbates myocardial damage and affects the prognosis of patients with ST-elevation myocardial infarction. This study investigates the potential cytoprotective effects of hemin in an in vitro cardiomyocyte model subjected to hypoxia/reoxygenation, a simulation of ischemia-reperfusion injury, building upon previous evidence of hemin's efficacy in modulating ischemia-reperfusion injuries in various biological tissues.
Methods: H9c2 cardiomyocytes were exposed to a simulated hypoxia/reoxygenation environment. The experimental setup included pretreatment with hemin at varying concentrations, with subsequent assessment in the presence and absence of a heme oxygenase-1 inhibitor (Zinc-Protoporphyrin IX (heme oxygenase-1 inhibitor)).
Results: Pretreatment with 5 μM hemin notably attenuated the oxidative stress and apoptosis in H9c2 cardiomyocytes following hypoxia/reoxygenation exposure, while simultaneously upregulating heme oxygenase-1 expression. This protective effect was found to be heme oxygenase-1 dependent, as evidenced by its attenuation upon the introduction of Zinc-Protoporphyrin IX (heme oxygenase-1 inhibitor), a heme oxygenase-1 inhibitor.
Conclusion: The findings suggest that low-dose, short-term hemin pretreatment can effectively reduce hypoxia/reoxygenation-induced cellular damage in cardiomyocytes through the upregulation of heme oxygenase-1. These results underscore the therapeutic potential of hemin in attenuating myocardial hypoxia/reoxygenation injury.