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.