Abstract

To research the effects of melatonin on cardiac function, myocardial cell metabolic stress and apoptosis in heart failure after myocardial infarction rats. Thirty specific-pathogen-free male Sprague Dawley rats were randomly divided into sham operation group (n=10), model group (n=10) and melatonin group (n=10). The model group and the melatonin group were constructed by ligating the left anterior descending coronary artery, while not in the sham operation group. Melatonin group (10 mg/kg) was intraperitoneally injected with melatonin (Sigma, United States of America) 30 min before operation. The sham operation group and the model group were injected intraperitoneally with the same amount of normal saline. The cardiac function of rats was measured by left ventricular ejection fraction, left ventricular fractional shortening, left ventricular end diastolic diameter and left ventricular end-systolic diameter. The myocardial cell apoptosis in ischemic areas of each group was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling staining. The expression of related proteins, measure myocardial fibrosis and determine the oxidative stress parameters (nicotinamide adenine dinucleotide phosphate oxidases activity, superoxide anion, malondialdehyde and superoxide dismutase) were detached via Western blot. Left ventricular fractional shortening % and left ventricular ejection fraction % in the melatonin group were significantly increased than those in the model group (p<0.05), while left ventricular end diastolic diameter and left ventricular end-systolic diameter in the melatonin group were significantly decreased (p<0.05). The apoptotic cardiomyocytes number in melatonin group was significantly less in model group (p<0.05). The levels of B-cell lymphoma 2 associated X-protein and caspase-3 protein in rat cardiomyocytes in melatonin group were significantly lower than those in model group (p<0.05). The proportion of sirius red staining in the melatonin group was significantly less than that in model group (p<0.05). Collagen I/III and transforming growth factor of rat cardiomyocytes in melatonin group-beta was significantly down-regulated than that in the model group (p<0.05). Nicotinamide adenine dinucleotide phosphate oxidase activity, superoxide anion and malondialdehyde level of rats in melatonin group were significantly decreased than those in model group, while superoxide dismutase activity was significantly increased than that in model group (p<0.05). Melatonin can improve heart failure and cardiac fibrosis by restraining oxidative stress in heart failure rats. Nicotinamide adenine dinucleotide phosphate oxidases 1 play an important role in regulating the role of melatonin in reducing cardiac fibroblasts fibrosis.