Abstract
Purpose Patients with diabetes are vulnerable to myocardial I/R (ischaemia/reperfusion) injury, but are not responsive to IPO (ischaemic post-conditioning). We hypothesized that decreased cardiac Adiponectin (APN) is responsible for the loss of diabetic heart sensitivity to IPO cardioprotecton.Methods Diabetic rats were subjected to I/R injury (30 min of LAD occlusion followed by 120 min of reperfusion). Myocardial infarct area was determined by TTC staining. Cardiac function was monitored by a microcatheter. ANP, 15-F2t-isoprostane, nitrotyrosine and MDA were measured by assay kits. Levels of p-Akt, total-Akt and GAPDH were determined by Western Blot.Results Diabetic rats subjected to myocardial IR exhibited severe myocardial infarction and oxidative stress injury, lower APN in the plasma and cardiac p-Akt expression ( P <0.05). IPO significantly attenuated myocardial injury and up-regulated plasma APN content and cardiac p-Akt expression in non-diabetic rats but not in diabetic rats. Linear correlation analysis showed that the expression of adiponectin was positively correlated with p-Akt and negatively correlated with myocardial infarction area ( P <0.01).Conclusion Protective effect of IPO was tightly correlated with the expression of adiponectin, exacerbation of I/R injury and ineffectiveness of IPO was partially due to the decline of adiponectin and inactivation of Akt in diabetes mellitus.
Highlights
IntroductionDiabetes mellitus (DM) has aroused increasing attention globally[1]
Over the last decades, diabetes mellitus (DM) has aroused increasing attention globally[1]
Studies have shown that myocardial ischemia-reperfusion injury was significantly increased in adiponectin gene knockout mice[7], and adiponectin level was significantly decreased in patients with DM, and they had a negative correlation with ischemic heart disease[8]
Summary
Diabetes mellitus (DM) has aroused increasing attention globally[1]. Studies have shown that myocardial ischemia-reperfusion injury was significantly increased in adiponectin gene knockout mice[7], and adiponectin level was significantly decreased in patients with DM, and they had a negative correlation with ischemic heart disease[8]. All these studies suggested that low adiponectin level might be one of the important mechanisms of the occurrence and development in diabetic patients with ischemic heart disease. We tested the relations of ANP expression to ischemia reperfusion injury, and investigated the potential mechanisms of ineffectiveness of ischemic postconditioning on diabetic myocardium ischemia reperfusion injury
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