We aimed to evaluate the effect of
melatonin on myo-cardial cell oncosis in the
myocardial ischemia/
reperfusion injury rat, and the role of the
mitochondrial permeability transition pore (MPTP) therein. Sprague Dawley rats (N = 60) were randomly divided into five groups of 12 rats each: control,
ischemia/reperfusion (I/R),
melatonin treatment (MT),
melatonin treatment +
atractyloside (MT+ATR), and
atractyloside (ATR). We prepared the
myocardial ischemia/reperfusion model by reperfusion after the left anterior descending coronary artery was ligated for 30 min. The MT rats were given
a 10 mg/kg MT intra-venous injection immediately thereafter; the MT+ATR rats were also given a 5 mg/kg ATR
intravenous injection 15 min before the
ischemia; the ATR rats were given the ATR injection only. After 2-h re-perfusion, myocardial tissue was extracted, the
infarction size was determined, and myocardial ultrastructures were observed using electron microscopy. The expression level of the preoncosis receptor (porimin), which can induce membrane injury, was determined by western blot; the
nicotinamide adenine dinucleotide (
NAD(+)) content was determined spectrophotometrically. The four treatment groups showed upregulat-ed expression of myocardial porimin, increased
myocardial infarction size, and reduced
NAD(+) content (P < 0.05). Compared with the I/R and MT+ATR groups, MT rats showed downregulated expression of myo-cardial porimin, reduced
myocardial infarct size, and increased myo-cardial cell
NAD(+) content (P < 0.05). The above indices between the ATR and MT+ATR groups were not significantly different (P > 0.05). Thus, MT might protect
myocardial ischemia/reperfusion rats by inhibiting
MPTP opening and reducing myocardial cell oncosis.