CD36 inhibition partially attenuates myocardial injury in diabetic rats with ischemic postconditioning

Abstract

IntroductionTo investigate the role of CD36 (fatty acid translocation enzyme) in the myocardial ischemia reperfusion (IR) injury in diabetes with ischemic postconditioning (IPostC).Research design and methodsAdult male Sprague-Dawley rats received streptozotocin treatment to establish type 1 diabetic model. After 8 weeks, diabetic rats were subjected to myocardial IR and IPostC with or without sulfo-N-succinimidyl oleate (SSO, an inhibitor of CD36) intervention.ResultsDiabetic rats showed the upregulation of myocardial CD36 expression and the increase in free fatty acid (FA) and triglycerides (TG) level and FA β oxidation (FAO). The cardioprotection of IPostC was compromised in diabetic rats with myocardial IR as evidenced by increased myocardial infarct size and plasma levels of lactate dehydrogenase (LDH), creatine kinase MB isoenzyme (CK-MB), and cardiac troponin Ⅰ (cTn-I), but not in non-diabetic rats with myocardial IR. SSO significantly decreased the levels of plasma LDH, CK-MB, cTn-I, free FA, and the levels of myocardial malondialdehyde, 8-isoprostane, FA, TG, and CD36 expression, and significantly increased the levels of myocardial glutathione peroxidase, total glutathione/oxidized glutathione, FAO, peroxisome proliferator activated receptor alpha, pyruvate dehydrogenase kinase 4, and the early (E) and late (A) diastolic filling ratio of heart in diabetic rats with IR and IPostC. However, no significant differences were observed in myocardial infarct size, heart rate, ejection fraction, fractional shorting, and dp/dtmax.ConclusionsCD36 downregulation partially attenuated myocardial IR injury in diabetic rats with IPostC via ameliorating FA metabolism and oxidative stress.