JAK-STAT通路在兔心肌缺血后处理中的作用

发布时间：2018-05-07 01:03

本文选题：心肌 + 缺血后处理　；参考：《临床荟萃》2014年12期

【摘要】：目的观察JAK-STAT通路在兔心肌缺血后处理(IPO)模型中的作用。方法将30只新西兰兔随机分为3组。组1缺血再灌注组(I/R组,n=10)只进行简单的缺血再灌注,即每只标本在阻断前降支30分钟后再进行120分钟的再灌注。组2单纯缺血后处理组(IPO组,n=10),给予IPO,不给予通道阻断剂。组3,进行IPO,同时给予JAK-STAT特异性阻断剂AG490(AG490+IPO组,n=10)。以阻断前10分钟为起点,期间每10分钟记录1次左心室压力情况。每组分别于阻断前、阻断后20分钟、再灌注后60分钟、120分钟抽取2ml血液作为标本,分别进行心肌磷酸激酶(CPK)的检测;最后处死,进行细胞凋亡检测。结果各组的CPK于缺血、再灌注后均明显增加,组2CPK于再灌注后较组1显著降低(P0.05),而组3与组1之间差异无统计学意义。±dp/dt max是反映左室收缩功能及舒张功能的重要指标,越靠近0点表明心功能越差,IPO对心功能起到了保护作用,而AG490阻断了IPO的保护作用。组2的细胞凋亡千分率均小于组1(P0.01),组3与组1差异无统计学意义。结论 IPO可以减少心肌细胞的坏死及凋亡、心肌酶的释放,改善心功能。JAK-STAT通路参与了IPO的保护机制。
[Abstract]:Objective To observe the role of JAK-STAT pathway in the model of rabbit myocardial ischemic postconditioning (IPO). Methods 30 New Zealand rabbits were randomly divided into 3 groups. Group 1 ischemia reperfusion group (group I/R, n=10) only performed simple ischemia-reperfusion, that is, each specimen was reperfusion for 30 minutes before blocking the anterior descending branch and after 120 minutes of reperfusion. Group 2 IPO group (group IPO) N=10), give IPO, do not give channel blockers. Group 3, IPO, and JAK-STAT specific blocker AG490 (AG490+IPO group, n=10). To block the first 10 minutes as the starting point, and record 1 times of left ventricular pressure every 10 minutes. Each group is blocked, 20 minutes after blocking, 60 minutes after reperfusion, and 120 minutes to extract 2ml blood as a specimen. The detection of cardiac phosphate kinase (CPK) was carried out, and the apoptosis was detected at last. Results the CPK of each group increased significantly after ischemia and reperfusion, and the group 2CPK was significantly lower than group 1 after reperfusion (P0.05), while the difference between group 3 and group 1 was not statistically significant. + dp/dt Max was an important indicator of the systolic and diastolic function of the left ventricle. The closer to the 0 point table, the worse the heart function was, the more IPO played a protective role in heart function, and AG490 blocked the protective effect of IPO. The percentage of apoptosis in group 2 was less than group 1 (P0.01), and there was no significant difference between group 3 and group 1. Conclusion IPO can reduce the necrosis and apoptosis of cardiac myocytes, release of myocardial enzymes and improve the.JAK-STAT pathway of cardiac function. Participate in the protection mechanism of IPO.

【作者单位】：邢台市第三医院心外科;河北医科大学第二医院心外科;邢台市人民医院外科;
【基金】：河北省科技支撑计划项目(2013ZC197)
【分类号】：R363

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