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American Journal of BioMedicine Volume 2, Issue 7, pages 799-810, July 2014
Najah R. Hadi; Fadhil G. Al-Amran; Maitham G. Yousif; suaad T. Zamil
Abstract
Myocardial ischemia and reperfusion (I/R) injury is known to occur on restoration of coronary flow after a period of myocardial ischemia. Angiotensin II (Ang II) is the most important bioactive substance of the renin-angioensin system (RAS), and exerts its physiological actions through AT1 receptors by regulating vascular tension and blood flow, and promoting cell growth and proliferation. The aim of the present study is to investigate the effects and its possible underlying mechanisms of AT1-AB on myocardial ischemia/reperfusion (I/R) injury. To test this hypothesis, we randomly assigned four groups (six mice per group) for experiment. To produce myocardial injury, the left anterior coronary artery (LAD) was occluded for 30 min, followed by 120 min of reperfusion in anesthetized mice. In the mice heart subjected to I/R injury, pretreatment AT1-AB (1mcg/gm) decreased the pathological scores of myocardium, and significantly attenuated I/R-induced increases of myocardial TNFα, IL-1β, IL-6. Further, 1mcg/gm AT1-AB significantly attenuated cTn-I and reduced apoptosis index of cardiac muscle cell of mice subjected to I/R injury. Therefore, these results demonstrate that AT1-AB exhibits significant protective effect against myocardial I/R injury which is related to inhibition of the release of inflammatory cytokines and the apoptosis of cardiac muscle cell.
Keywords: AT1-AB; Ischemia/reperfusion; cTn-I; Pro-inflammatory cytokine; Apoptosis
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