Electron transfer flavoprotein subunit beta suppresses hypoxia/reoxygenation-induced mitochondrial dysfunction and apoptosis in cardiomyocytes

ischemia-reperfusion model was established in H9c2 cardiomyocytes using hypoxia/reoxygenation. Myocardial injury was assessed by measuring the levels of creatine kinase-MB, cardiac troponin I, cardiac troponin T, and lactate dehydrogenase. Apoptosis was evaluated via terminal deoxynucleotidyl transferase dUTP nick-end labeling staining and Annexin V-PE/7-AAD flow cytometry. Mitochondrial morphology was observed via transmission electron microscopy, while mitochondrial function was assessed by measuring reactive oxygen species and membrane potential. Oxidative stress markers and apoptosis-related proteins were also assessed.ResultsHypoxia/reoxygenation treatment significantly increased the levels of myocardial injury markers and downregulated electron transfer flavoprotein subunit beta expression. The model group exhibited enhanced apoptosis, impaired mitochondrial structure, elevated reactive oxygen species levels, reduced mitochondrial membrane potential, and increased oxidative stress. Overexpression of electron transfer flavoprotein subunit beta effectively reversed these changes: it reduced the injury markers, decreased apoptosis, improved mitochondrial morphology and function, attenuated oxidative stress, and modulated the expression of apoptosis-related proteins.ConclusionsElectron transfer flavoprotein subunit beta protects against myocardial ischemia-reperfusion injury by ameliorating mitochondrial dysfunction, reducing oxidative stress, and inhibiting apoptosis, identifying it as a potential therapeutic target.