Hemin as a protective agent in an in vitro model of hypoxia/reoxygenation-induced injury.

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.