| Background Coronary heart disease(CHD) is the leading cause of death and disability worldwide, but there is still no very effective therapy for preventing myocardial ischemia reperfusion injury. Growing evidence indicates that oxidative stress and myocardial apoptosis play an important role in I/R-induced injury. Various reports suggest that antioxidant and antiapoptotic therapy would help the myocardium to recover from I/R-mediated tissue damage and dysfunction. Soybean oligosaccharides(SO), which are isolated from the soybean seeds, have been shown to be a promising candidate for the prevention of many diseases particularly those triggered by oxidative stress. However, the effects of SO on myocardial I/R injury and the machanism remain not clear.Objective The aim of the present study was to investigate whether SO protects heart function against myocardium ischemia reperfusion injury and to find out its mechanism using a MIR rat model.1.To identify whether SO can attenuate myocardial I/R injury and show its cardioprotective effect;2.To determine whether SO can reduce oxidative stress in myocardial I/R injury;3.To investigate the effect of SO on myocardial apoptosis induced by myocardial I/R injury;4.To evaluate the potential role of JAK2/STAT3 pathway against myocardial I/R injury and the effect of SO on JAK2/STAT3 pathway.Methods1.Rats were fed for 30 days with saline(sham and MIR groups) or the SO(200 or 400mg/kg body weight, daily). At the end of 30 days, the left anterior descending coronary artery was occluded for 30 min, followed by 24 h reperfusion in anesthetized rats. Sham operated animals were subjected to the same surgical procedures, except that the suture under the left anterior descending coronary artery was not tied;2.The hemodynamic parameters were analyzed by ALC –MPA Biological Signal Analysis System;3.The pathologic morphology was observed by HE staining; The changes of myocardial ultrastructure was observed by electron microscope;4.Measurement of myocardial infarct size were evaluated by Evans Blue/TTC staining;5.The activity of AST, CK-MB and LDH were analyzed using commercial kits by employing an autoanalyzer;6.The lever of MDA was analyzed by the thiobarbituric acid assay; SOD activity was analyzed by xanthine oxidase;The activity of GSH-Px and GSH was assayed by Chemical colorimetric method; CAT activity was measured by ultraviolet spectrophotometric method.Specific Steps were performed in accordance with the kit instructions;7.Na+–K+–ATPase and Ca2+–Mg2+–ATPase activities were assayed by chemical colorimetric method;8.TUNEL staining was performed to evaluate the myocardial apoptosis index according to the manufacturer’s instructions;9.Western blotting assay was performed to determine the expression of apoptosis-related protein including Bax,Bcl-2 and Cleaved caspase-3;10.Western blotting assay was performed to determine the expressions of JAK2, p-JAK2,STAT3 and p-STAT3 following standard protocol.Result Pretreated with SO, it showed a significant recovery in cardiac contractile function, reduction in infarct size and myocardial apoptosis,and also decrease in CK-MB,AST and LDH activities. SO decreased MDA level, increased antioxidant enzymes activities and Na+–K+–ATPase, Ca2+–Mg2+–ATPase activities in the SO-treatment group.Moreover, SO also significantly increased the expression of p-JAK2 and p-STAT3 proteins in rat heart. However, no significant change in JAK2 and STAT3 levels was observed.Conclusion SO has a positive protective action against I/R-induced myocardium damage in rats, as assessed by oxidative stress,myocardial apoptosis, myocardial enzymes and infarction size. In addition, SO has beneficial effects in myocardium ischemia reperfusion injury with a potential mechanism of activating the JAK2/STAT3 signal pathway and more study is needed for clinical tests in the future. |
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