Abstract

Background: Myocardial ischemia–reperfusion represents a clinically relevant problem associated with thrombolysis, angioplasty and coronary bypass surgery. Injury of myocardium due to ischemia–reperfusion includes cardiac contractile dysfunction, arrhythmias as well as irreversible myocytes damage.Objective: This study was undertaken to investigate the potential role of simvastatin in amelioration of myocardial I/R injury induced by ligation of coronary artery in a rat model. Materials & methods: adult male Swiss Albino rats were randomized into 4 equal groups. Group (I) sham group: rats underwent the same anesthetic and surgical procedure as the control group except ligation of LAD coronary artery , Group(II) control group: rats subjected to regional ischemia for 25 min by ligation of LAD coronary artery and reperfusion for 2 hours ,Group(III ) control vehicle group: rats received vehicle of simvastatin (normal saline) via I.P injection and subjected to regional ischemia for 25 min by ligation of LAD coronary artery and reperfusion for 2 hours , Group(IV) simvastatin treated group :rats pretreated with simvastatin 1mg/kg i.p 1 hr before ligation of LAD coronary artery. At the end of experiment (2 hr of reperfusion), the heart was harvested and the part of the heart just below the site of ligation was divided into two parts ,the upper part was homogenized for the measurement of interleukin-1β (IL-1β) and the lower part of tissues fixed in 10% formalin and embedded in paraffin the sections were stained with hematoxylin and eosin (H&E) then used for histopathological study .Results: Compared with the sham group, levels of myocardial IL-1β, were increased (p<0.001) in the control group. Simvastatin significantly counteract the increase in myocardium level of IL-1B (P < 0.001). Histological analysis revealed that simvastatin markedly reduced (P < 0.001) the severity of cardiac injury in the rats underwent LAD ligation procedure .Conclusions:The results of the present study reveal that simvastatin may ameliorate myocardial I/R injury in rats via interfering with inflammatory responses which induced by I/R injury.

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