The disappearance of IPO in myocardium of diabetes mellitus rats is associated with the increase of succinate dehydrogenase-flavin protein

Abstract

Background The aim of the present study was to investigate whether the disappearance of ischemic post-processing (IPO) in the myocardium of diabetes mellitus (DM) is associated with the increase of succinate dehydrogenase-flavin protein (SDHA). Methods A total of 50 Sprague Dawley rats, weighing 300–400 g, were divided into 5 groups according to the random number table method, each with 10 rats. After DM rats were fed a high-fat and -sugar diet for 4 weeks, they were injected with Streptozotocin to establish the diabetic rat model. Normal rats were fed the same regular diet for the same number of weeks. Next, the above rats were taken to establish a cardiopulmonary bypass (CPB) model. Intraperitoneal glucose tolerance test (IPGTT) and oral glucose tolerance test (OGTT) were used to detect whether the DM rat model was established successfully. Taking blood from the femoral artery to collect the blood-gas analysis indicators, and judged whether the CPB model is established. After perfusion was performed according to the experimental strategy, the area of myocardial infarction (MI), and serum creatine kinase isoenzyme (CK-MB) and cardiac troponin (CTnI) levels were measured. Finally, the relative mRNA and protein expression of SDHA was detected. Results The OGTT and IPGTT suggested that the DM rat model was successfully established. The arterial blood gas analysis indicated that the CPB model was successfully established. As compared with the N group, the heart function of the IR group was significantly reduced, the levels of myocardial enzyme markers, the area of MI, as well as the relative mRNA and protein expression of SDHA, were all increased. As compared with the IR group, the CK-MB and CTnI levels in the IPO group, the MI area, relative mRNA and protein expression of SDHA decreased. As compared with the IPO group, the myocardial enzyme content in the DM + IPO group, the MI area and the relative mRNA and protein expression of SDHA increased. As compared with the DM + IPO group, in the DM + IPO + dme group, the myocardial enzyme content, area of MI and relative mRNA and protein expression were all decreased. Conclusion IPO can inhibit the expression of SDHA, reduce MIRI and exert a cardioprotective effect in the normal rats. However, the protective effect of IPO disappears in the diabetic rats. The inhibitor dme combined with IPO can increase the expression of SDHA and restore the protective effect of IPO in DM myocardia.

A study on the relationship between succinate dehydrogenase and mitoKATPC in the mechanism of ischemic postconditioning protecting against MIRI under CPB in adult rats

“…Once tissue perfusion is restored, excess SA will trigger a burst of ROS, resulting in myocardial tissue reperfusion injury. The research group established an isolated rat cardiac ischemia-reperfusion model in the early stage and found that the main functional subunit of SDH, the expression of succinate dehydrogenase avoprotein (SDHA), was abnormally increased during the reperfusion period, IPO group SDHA protein expression was signi cantly reduced, inhibiting SDHA activity can improve MIRI cardiac function in isolated rats [14] . The above studies suggest that increased SDH activity is involved in the occurrence of MIRI, and can be used as a target for IPO to play a cardioprotective role, but how does IPO inhibit SDHA expression and SDH activity to play a role in MIRI cardio-protection?…”