ArticleSAGE open medicine2025
Hemin as a protective agent in an in vitro model of hypoxia/reoxygenation-induced injury.
Article in SAGE open medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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2 authors.
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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.
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