JAK-STAT通路在兔心肌缺血后处理中的作用  

Effect of JAK-STAT pathway on myocardial ischemic post-conditioning in rabbit hearts

作　　者：付长江 刘苏[2] 郭立新 闫世伟 左相荣[3] 李瑞冰 

机构地区：[1]邢台市第三医院心外科,河北邢台054000 [2]河北医科大学第二医院心外科,河北石家庄050000 [3]邢台市人民医院外科,河北邢台054000

出　　处：《临床荟萃》2014年第12期1385-1388,1394,共5页Clinical Focus

基　　金：河北省科技支撑计划项目(2013ZC197)

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(P<0.05),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(P<0.01),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。Objective To explore the effect of JAK-STAT pathway on myocardial ischemic postconditioning （IPO） in vivo model of rabbit heart. Methods Thirty rabbits were randomly divided into three groups. Group 1 （ischemic/reperfusion, I/R, n = 10） ：the left anterior descending（LAD） of each rabbit heart was reperfused for 120 rain after being occluded for 30 rain. Group 2 （ischemic postconditioning, IPO, n = 10）.. before the 120 min reperfusion,the LAD was loosen and cut off every 30 s, for 3 times. Group 3 （AG490＋ IPO, n = 10） ： like group 2,the difference was given tyrosine inhibitor AG490. Taken the time before occlusion 10 rain as starting point, every 10 rain, we recorded left ventricle pressure in the procedure of ischemie reperfusion. Through collecting 2 ml blood as a sample at the specified time,creatine phosphatekinase（CPK） was detected. After the experiment was completed, all hearts were detected for the apoptosis on the myocardium. Results The level of CPK in group 2 was significantly decreased compared to group 1 （ P 〈0.05）. There were no significant difference between group 1 and group 3. It has a bad heart function if ：t：dp/dt max approach to zero. The heart function in group 1 was downtrend compared with group 2. In group 3,the heart function was downtrend,too. The cadiocyte apoptosis of group 1 and group 3 was higher than that of group 2. The statistical results showed that the contrast between group 1 and group 2 was significant（ P 〈0.05） ;there were no significant difference between group 1 and group 3. Conclusion IPO can reduce the release of CPK, necrosis and apoptosis of cell; improve the heart function. The JAK-STAT pathway participates the protection mechanism of IPO.

关 键 词：心肌 缺血后处理 JAK-STAT信号通路 阻断剂 

分 类 号：R33[医药卫生—人体生理学]