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Effect of melatonin on oncosis of myocardial cells in the myocardial ischemia/reperfusion injury rat and the role of the mitochondrial permeability transition pore.

Abstract
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.
AuthorsL F Liu, Z H Qian, Q Qin, M Shi, H Zhang, X M Tao, W P Zhu
JournalGenetics and molecular research : GMR (Genet Mol Res) Vol. 14 Issue 3 Pg. 7481-9 (Jul 06 2015) ISSN: 1676-5680 [Electronic] Brazil
PMID26214427 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Mitochondrial Membrane Transport Proteins
  • Mitochondrial Permeability Transition Pore
  • Receptors, Cell Surface
  • NAD
  • Melatonin
Topics
  • Animals
  • Male
  • Melatonin (pharmacology)
  • Mitochondrial Membrane Transport Proteins (metabolism)
  • Mitochondrial Permeability Transition Pore
  • Myocardial Infarction (metabolism, pathology)
  • Myocardial Reperfusion Injury (metabolism, pathology)
  • Myocardium (pathology, ultrastructure)
  • NAD (metabolism)
  • Rats, Sprague-Dawley
  • Receptors, Cell Surface (metabolism)

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