电针对脑缺血大鼠缺血灶区信号转导与转录激活子3表达的影响

摘要

目的:研究信号转导与转录激活子3(STAT 3),在脑缺血后不同时间段的变化、信号转导以及电针的干预作用.方法:采用随机数字表法将150只SD大鼠随机分为假手术组、模型组和电针组,每组又分为2h、1d、3d、1周和3周5个时间段组,共15组.电凝闭大鼠大脑中动脉制作局灶性脑缺血模型.电针组电针刺激“百会”“大椎”穴,每次30 min,每日1次.采用免疫组化和蛋白印迹的方法检测大鼠缺血侧皮质区STAT 3表达水平.结果:局灶性脑缺血2h后,模型组和电针组STAT 3表达水平开始增加,但两组间差异无统计学意义(P＞0.05).缺血1d后,STAT 3水平达到高峰,电针组与模型组的差异具有统计学意义(P＜0.001),电针能下调脑缺血后病灶区STAT 3水平的表达,且这种效应一直持续到脑缺血3周(P＜0.001,P＜0.05).结论:电针治疗可以通过下调脑缺血后病灶区STAT 3表达水平,持续地参与机体的自我保护机制.%Objective To observe the effect of electroacupuncture CEA) intervention on expression of signal transducer and activator of transcription 3 (STAT 3) in the focal ischemic cerebral tissue, so as to study its mechanism underlying improving ischemic stroke. Methods A total of 150 SD rats were randomized into sham operation (control) group, cerebral ischemia (CD model (model) group and EA group which were further randomly divided into 2 hour (2 h), 1 day (1 d), 3 d, 1 week (1 W) and 3 W subgroups (n=6/sobgroup.for immunohistochemistry, n = 4/subgroup for Western blot). Cl model was established by occlusion of the middle cerebral artery with electro-coagulation method. EA (3 Hz/20 Hz, 2-3 V) was applied to "Baihui" (GV20) and "Dazhui "(GV 14) for 30 min. The expression of cerebral STAT 3 was detected by immunofluorescence histochemistry and laser-confocal microscopy, and Western blot, separately. Results Compared with the control group, cerebral STAT 3 immunofluorescence intensity values at the time-points of 2 h, 1 d, 3 d and 1 W, STAT 3 protein expression levels at the time-points of 2 h, 1 d and 3 d in the model group were increased significantly (P<0. 001, P<0. 05). After acupuncture intervention, cerebral STAT 3 immunofluorescence intensity values at the time-points of 1 d. 3 d, 1 W and 3 W, STAT 3 protein expression levels at the time-points of t d, 3 d and 3 W in the EA group were down-regulated considerably (P<0. 001, P<0. 01, P<0. 05). No significant differences were found between the control and model groups in STAT 3 immunofluorescence intensity at 3 W, and in STAT 3 protein expression levels at 1 W and 3 W, and between the EA and model groups in STAT3 immunofluorescence intensity at 2 h, and in STAT 3 protein expression at 2 h, 3 d and 1 W (P>0.05). Conclusion EA therapy can down-regulate the expression level of STAT 3 protein in the regional ischemic cerebral tissue in cerebral ischemia fats, which may contribute to its efficacy in the treatment of acute and chronic ischemic stroke.