Melatonin protects against isoproterenol‐induced alterations in cardiac mitochondrial energy‐metabolizing enzymes, apoptotic proteins, and assists in complete recovery from myocardial injury in rats

摘要: The present study was undertaken to explore the protective effect of melatonin against isoproterenol bitartrate (ISO)-induced rat myocardial injury and test whether has a role in preventing recovery when ISO-induced stress is withdrawn. Treatment for rats with ISO altered activities of some key mitochondrial enzymes related energy metabolism, levels proteins, the proteins related apoptosis. These changes were found be ameliorated when animals pretreated at dose 10 mg/kg BW, i.p. In addition its ability reduce mitochondrial dysfunction, we also studied the cardiac tissue after damage. Continuation melatonin treatment rats withdrawal treatment reduce the cardiac injury biomarkers including serum glutamate oxaloacetate transaminase (SGOT), lactate dehydrogenase (LDH), and cardio-specific LDH1 control levels. lipid peroxidation and reduced glutathione brought back that seen control animals by continued treatment. post-ISO period improve cardiac tissue morphology heart function. Thus, findings indicate melatonin�s provide cardio protection low pharmacological dose process. Melatonin, molecule very low or no toxicity may considered as therapeutic for for ischemic disease.