中文摘要：

目的 探讨磷酸肌醇3激酶（PI3K）/蛋白激酶B（Akt）和Janus蛋白酪氨酸激酶（JAK）/信号转导与转录激活因子（STAT）信号转导通路在迷走神经电刺激后处理、肢体远隔缺血后处理以及迷走神经电刺激后处理联合肢体远隔缺血后处理减轻大鼠心肌缺血再灌注损伤中的作用.方法 雄性SD大鼠20只,8周龄,体重290 ～ 320 g,采用随机数字表法,将其分为4组（n=5）：缺血再灌注组（1/R组）、迷走神经电刺激后处理组（EVSP组）、肢体远隔缺血后处理组（RLIP组）、迷走神经电刺激后处理联合肢体远隔缺血后处理组（EVSP-RLIP组）.采用结扎冠状动脉左前降支30 min再灌注60 min的方法制备心肌缺血再灌注模型.EVSP组和EVSP-RLIP组在心肌缺血15 min时对右侧迷走神经干实施电刺激30 min,参数设置：波宽1 ms,频率10 Hz、刺激电流随大鼠HR进行调整,以保持HR较刺激前降低10％.RLIP组和EVSP-RLIP组在心肌缺血20 min时采用止血带结扎双后肢10 min后恢复血流灌注行肢体远隔缺血后处理.缺血再灌注期间记录血流动力学指标.再灌注60 min时采集颈静脉血样,采用酶联免疫吸附法检测血清肌钙蛋白I（cTnI）和MB型肌酸激酶同工酶（CK-MB）的浓度；处死动物,取缺血区和非缺血区心肌组织,采用Western blot法检测磷酸化Akt（p-Akt）和磷酸化STAT3（p-STAT3）蛋白的水平；采用RQ-PCR法检测Akt和STAT3 mRNA的表达水平.结果 与IR组比较,POES组、LRIP组和POES-LRIP组缺血再灌注期间HR降低,血清cTnI和CK-MB浓度降低,缺血区和非缺血区心肌p-Akt和p-STAT3蛋白表达上调,EVSP-LRIP组缺血区和非缺血区心肌Akt和STAT3的mRNA表达上调（P＜0.05）.与EVSP组和LRIP组比较,EV SP-LRIP组血清CK-MB浓度降低,缺血区和非缺血区心肌p-Akt、p-STAT3蛋白表达及Akt和STAT3的mRNA表达上调（P＜0.05）.结论 PI3K/Akt和JAK/STAT信号转导通路激活后介导了迷走神经电刺激后处理、肢?

英文摘要：

Objective To investigate the roles of phosphatidylinositol 3-kinase（PI3K）/protein-serine-threonine kinases （Akt） and Janus kinase/signal transducer and activator of transcription （JAK/STAT） signal transduction pathways in reduction of myocardial ischemia-reperfusion（I/R） injury by electric vagal stimulation postconditioning （EVSP）,remote limb ischemic postconditioning （RLIP） or EVSP combined with RLIP （EVSP-RLIP） in rats.Methods Twenty male Sprague-Dawley rats,weighing 290-320 g,were randomly allocated into 4 groups （n=5 each）：I/R group,EVSP group,RLIP group and EVSP-RLIP group.Myocardial I/R was induced by occlusion of left anterior descending branch of coronary artery for 30 min followed by 120 min reperfusion.In EVSP and EVSP-RLIP groups,the right vagus nerve was stimulated for 30 min with continuous electric rectangular pulses （2 ms,10 Hz,1-2 V） starting from 15 min of ischemia,and the voltage of the pulses was adjusted to decrease HR by 10％ of the baseline HR before stimulation.In RLIP and EVSP-RLIP groups,the animals underwent 10 min ischemia of bilateral hind limbs starting from 20 min of myocardial ischemia.The parameters of hemodynamics were recorded during I/R.At 60 min of reperfusion,the blood samples were taken from the jugular vein for determination of serum cardiac troponin I （cTnI） and creatine kinase MB （CK-MB） concentrations （by ELISA）,and then the rats were sacrificed and myocardial specimens were obtained from both the ischemic and non-ischemic regions for determination of the levels of phosphorylated Akt （p-Akt） and phosphorylated STAT3 （p-STAT3） （by using Western blot） and expression of Akt and STAT3 mRNA （by RQ-PCR）.Results Compared with I/R group,HR during I/R and serum cTnI and CK-MB concentrations were significantly decreased,and the levels of myocardial pAkt and p-STAT3 were increased in both ischemic and non-ischemic regions in EVSP,RLIP and EVSP-RLIP groups,and the expression of Akt and STAT3 mRNA in both ischemic and