Akkoc H.Tunik S.Kelle I.Gurkan A.Erdogmus Z.Simsek S.Erdinc M.2024-04-242024-04-2420130326-2383https://hdl.handle.net/11468/24845The aim of the present study was to investigate the protective effect of ethyl pyruvate (EP) against ischemia reperfusion (I/R) injury in isolated rat heart. Male Sprague-Dawley rats were divided into three groups (n = 8); Group 1: Control group, Group 2: I/R, Group 3: I/R+EP. Ischemia was produced for 30 min by blocking the perfusion with Krebs Henseleit solution and it was followed by reperfusion for 60 min. In group 3, EP (2 mmol/L) was added into Krebs Henseleit solution after stabilization period. EP did not change the number of ?-smooth muscle actin positive vessels and expression of Bcl-2 and desmin. Treatment with EP significantly reduced I/R induced extension in infarct size (p < 0.001) and release of lactate dehidrogenase (p < 0.001) and creatine phosphokinase (p < 0.05). Myocardial I/R injury significantly increased oxidative stress index and malondialdehyde, total oxidant status levels and significantly decreased paraoxonase actvity and total antioxidant status (p < 0.05). On the other hand, alterations in these biochemical indices due to I/R injury were attenuated by EP treatment (p < 0.01). These results show that ethyl pyruvate prevents ischemia reperfusion injury in isolated perfused rat heart.eninfo:eu-repo/semantics/closedAccessApoptosisEthyl PyruvateInfarct SizeMyocardial Reperfusion İnjuryOxidative StressArticle3233643702-s2.0-84878688226Q4