| Objective: Myocardial ischemia-reperfusion injury has attracted much attention in clinical work,which can lead to many complications and seriously affect the prognosis of patients with ischemic cardiomyopathy.In recent years,postconditioning is an important measure to prevent myocardial ischemia-reperfusion injury.It can improve the cardiac function of patients by reducing the size of myocardial infarction,reducing the occurrence of reperfusion arrhythmia,and alleviating microvascular reperfusion injury.c-Jun N-terminal Kinase(JNK)is an important member of mitogen-activated protein kinases.The activation of JNK signaling pathway triggers a series of pathophysiological processes,aggravating myocardial ischemia-reperfusion injury.It has been proved that postconditioning can protect rat kidney from ischemia-reperfusion injury by inhibiting the activation of JNK signaling pathway.It is concluded that whether the mechanism of myocardial protection after myocardial ischemic is related to the regulation of JNK signaling pathway and how JNK plays a role in mitigating myocardial ischemia-reperfusion injury after myocardial ischemic.In this study the expression levels of JNK were observed by constructing a rat model of myocardial ischemia-reperfusion injury with postconditioning as the intervention method.The role of JNK signaling pathways in mitigation of myocardial ischemia-reperfusion injury was preliminarily explored.The study can enrich the myocardial protective mechanism of myocardial ischemia postconditioning,and provide theoretical support and mechanism guarantee for clinical prevention and treatment of myocardial ischemia-reperfusion injury and search for new drug targets of cardioprotective effect.Methods: A total of sixty healthy male rats(8 weeks old,weighing 200-250g)were randomly allocated to one of the 6 groups(n=10)as follows: i)The sham group;ii)ischemia-reperfusion injury alone(I/R group);iii)ischemia-reperfusion with postconditioning(Post C group);iv)ischemia-reperfusion with the JNK inhibitor-SP600125(I-JNK group);v)ischemia-reperfusion with anisomycin(Ani group);and vi)post C and treatment with anisomycin(Ani+Post C group).The rat model of myocardial ischemia-reperfusion injury was established by clipping-releasing left coronary artery,and different treatments were given according to different experimental groups.At the end of treatment,serum samples were collected and the levels of myocardial injury markers were detected by creatinine kinase-muscle/brain(CK-MB)and troponin I kits.The myocardial infarction area was observed and analyzed by 2,3,5-triphenyl tetrazolium chloride(TTC)staining.Total protein was extracted from myocardium and the expression levels of phosphorylated JNK(P-JNK)were determined by Western blot.Results: i)The levels of CK-MB,Tn I and the infarct size were significantly higher in the I/R group than those in the Sham group(P<0.05).The levels of CK-MB,Tn I and the infarct size were significantly lower in the Post C group,I-JNK group and I-p38 group than those in the I/R group(P <0.05).Compared with the Post C group,the levels of CK-MB,Tn I and the infarct size were significantly higher in the Ani+Post C group and Ani group(P<0.05).ii)Compared with the Sham group,the expression levels of P-JNK were significantly higher in the I/R group(P < 0.05).Post C and I-JNK inhibited the production of P-JNK(P<0.05),while Ani promoted the increase of P-JNK(P<0.05).Compared with the Post C group,the expression levels of P-JNK were significantly higher in the Ani+Post C group and Ani group(P<0.05).Conclusion: i)Myocardial ischemia reperfusion has significant myocardial damage.Myocardial ischemia-reperfusion injury activates the JNK signaling pathway and promotes the expression of P-JNK.ii)Myocardial ischemia postconditioning can reduce the level of myocardial injury markers and decrease the size of myocardial infarction,to play a significant role in myocardial protection.iii)Myocardial ischemia postconditioning reduces the expression of P-JNK,and alleviates myocardial ischemia-reperfusion injury by inhibiting the JNK signaling pathway.iv)The JNK signaling molecular may be the target of myocardial ischemia postconditioning to reduce myocardial ischemia reperfusion injury and exert cardiac protective effects. |
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