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The role of nitric oxide, reactive oxygen species, and protein kinase C in oxytocin-induced cardioprotection in ischemic rat heart

Faghihi, M. and Alizadeh, A.M. and Khori, V. and Latifpour, M. and Khodayari, S. (2012) The role of nitric oxide, reactive oxygen species, and protein kinase C in oxytocin-induced cardioprotection in ischemic rat heart. Peptides, 37 (2). pp. 314-319. ISSN 01969781 (ISSN)

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Abstract

Ischemia-reperfusion injury is a common complication of heart disease that is the leading cause of death worldwide. Here, we plan to elucidate oxytocin cardioprotection effects against ischemia-reperfusion via nitric oxide (NO), reactive oxygen species (ROS), and protein kinase C (PKC) in anesthetized rat preconditioned myocardium. Forty-eight Sprague-Dawley rats were equally divided into eight groups. All animals were subjected to 25 min ischemia and 120 min reperfusion. Oxytocin (OT), L-NAME (LNA, a nitric oxide synthase inhibitor), chelerythrine (CHE, a PKC enzyme inhibitor), and N-acetylcysteine (NAC, a ROS scavenger) were used prior to ischemia. Results showed that mean arterial pressure significantly reduced during the first 10 min of ischemia and reperfusion in IR, LNA, CHE, and NAC groups (p < 0.05). OT prevented mean arterial pressure decline during early phase of ischemia and reperfusion. Cardioprotective effects of OT in infarct size, plasma levels of creatine kinase-MB and lactate dehydrogenase, severity and incidence of ventricular arrhythmias were abolished by L-NAME, chelerythrine, and N-acetylcysteine (p < 0.05). The present study showed that OT pretreatment reduces myocardial infarct size and ventricular arrhythmias, and improves mean arterial pressure via NO production, PKC activation, and ROS balance. These findings provide new insight into therapeutic strategies for ischemic heart disease. © 2012 Elsevier Inc.

Item Type: Article
Additional Information: Unmapped bibliographic data: LA - English [Field not mapped to EPrints] J2 - Peptides [Field not mapped to EPrints] C2 - 22902709 [Field not mapped to EPrints] AD - Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran [Field not mapped to EPrints] AD - Cancer Research Center, Cancer Institute of Iran, Imam Khomeini Hospital, Keshavarz Blvd., Tehran, Iran [Field not mapped to EPrints] AD - Department of Pharmacology, Golestan Cardiovascular Research Center, Golestan University of Medical Sciences, Gorgan, Iran [Field not mapped to EPrints] AD - Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran [Field not mapped to EPrints] AD - Islamic Azad University, Tehran Medical Beranch, Tehran, Iran [Field not mapped to EPrints] DB - Scopus [Field not mapped to EPrints]
Uncontrolled Keywords: Cardioprotection, NO, Oxytocin, PKC, ROS, acetylcysteine, chelerythrine, creatine kinase MB, lactate dehydrogenase, n(g) nitroarginine methyl ester, nitric oxide, oxytocin, protein kinase C, reactive oxygen metabolite, animal experiment, animal model, animal tissue, article, cardiovascular risk, controlled study, disease severity, drug effect, drug mechanism, enzyme activation, heart arrhythmia, heart hemodynamics, heart infarction size, heart muscle ischemia, heart protection, heart ventricle fibrillation, heart ventricle tachycardia, male, nonhuman, priority journal, rat, reperfusion injury, Animals, Male, Myocardial Ischemia, Nitric Oxide, Oxytocin, Protein Kinase C, Rats, Rats, Sprague-Dawley, Reactive Oxygen Species, Animalia, Rattus
Subjects: مقالات نمایه شده محققین دانشگاه در سایت ,Web of Science ,Scopus
موارد کلی
Divisions: معاونت تحقیقات و فناوری
Depositing User: GOUMS
Date Deposited: 20 Apr 2015 05:53
Last Modified: 25 Oct 2016 07:59
URI: http://eprints.goums.ac.ir/id/eprint/1967

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