To explore the mechanism of the protective effect of phosphocreatine on mitochondrial membrane potential in cardiomyocytes

Objective:To observe the protective effect of phosphocreatine on mitochondrial membrane potential in rat cardiomyocytes. Methods: Using H₂O₂ to cause oxidatie stress, CP was given ten minutes before H₂O₂ stimulation.JC-1 in combination with flow cytometry was used to measure the changes of mitochondrial membrane potential. Apoptosis was identified by means of double fluorescence staining with Annexin V-FITC/propidim iodide and TUNEL staining. The protective effect of CP was also appraised after rotenone and iodoacetamide （IA） was given to inhibit respiratory chain and CK enzyme respectively. Results: H₂O₂ caused the decrease of mitochondrial membrane potential and the increase of apoptosis rate. But in the CP treatment group, mitochondrial membrane potential wasn't decreased significantly. This protective effect disappeared after respiratory chain and CK enzyme was inhibited.Conclusions: CP can prevent the cardiomyocyte from oxidative injury. The mechanism may rely on inhibiting the decrease of mitochondrial membrane potential and protecting mitochondrial function.