The protective effect of tetramethylpyrazine on rat myocytes with transient oxygen-glucose deprivation followed by reoxygenation injury and mechanism study
Objective This study explored the protective effect of tetramethylpyrazine on myocardial ischemia/reperfusion injury via inhibiting oxidative stress. Methods Primary cultured neonatal myocytes were applied to explore the anti-ischemia/reperfusion injury property in vitro. The survival viability of myocytes was determined by MTT; enzyme activities such as lactate dehydrogenase, creatine kinase, superoxide dismutase, malondialdehyde, and nitric oxide were analyzed with assay kits; inducible nitricoxide synthase and endothelial nitric oxide synthase expressions were determined by Westernblot. Results Tetramethylpyrazine significantly improved the beating frequencies of myocytes after oxygen-glucose deprivation/reoxygenation procedure, decreased lactate dehydrogenase, creatine kinase, and malondialdehyde levels and enhanced superoxide dismutase activity.Tetramethylpyrazine also inhibited excessive production of nitric oxide through downregulating inducible nitric oxide synthase as well as upregulating endothelial nitric oxide synthase during ischemia/reperfusion injury. Conclusion Tetramethylpyrazine could significantly improve the oxidative-stress tolerance of myocytes to keep cell membrane integrity and protect the myocardial tissue of normal physiological function via an antioxidant effect and by restoring the balance between inducible nitric oxide synthase and endothelial nitric oxide synthase, while inhibiting the generation of cytotoxic concentrations of NO.
tetramethylpyrazinemyocytesoxidative stressoxygen-glucose deprivation/reoxygenationprotective effect and mechanism
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维普
