电针对局灶性脑缺血再灌注大鼠受损神经元细胞外信号调节蛋白激酶的影响

目的:探索电针对脑缺血再灌注大鼠大脑受损神经元的保护作用及其细胞外信号转导机制。方法:随机将24只SD大鼠均分为假手术组、模型组、电针组和电针+PD98059组,采用改良Longa线栓法复制局灶性大脑中动脉缺血再灌注模型。电针组取"百会"大椎"穴,选用疏密波,频率80～100Hz,电流强度1～3mA,电压1～3V,持续电刺激60min。电针+PD98059组于腰椎间隙注入丝裂原活化蛋白激酶1的抑制剂PD980592.78mg/kg,并电针。依据Julio氏神经行为学评分法对各组大鼠进行评分,采用免疫组织化学染色法观察电针及PD98059阻滞状态下电针对模型大鼠右侧病灶处颞叶大脑皮层锥体细胞层细胞外信号调节蛋白激酶(ERK)蛋白表达的影响。结果:电针能改善模型大鼠的神经行为学分值(P<0.01),上调脑缺血再灌注大鼠受损神经元ERK的蛋白表达(P<0.01),其作用可被PD98059阻断(P<0.01)。结论:电针可减轻脑缺血再灌注大鼠大脑神经元的损伤,促进损伤修复,这一作用可能与其影响缺血再灌注后ERK信号通路的变化有关。

Involvement of Extracellular Regulated Protein Kinase Signal Transduction Pathway in Electroacupuncture-induced Improvement of Ischemic Cerebral Injury in Rats with Cerebral Ischemia-reperfusion

Objective:To investigate the protective effect of electroacupuncture(EA)on ischemic cerebral neurons and the related intracellular signal transduction mechanism in rats with cerebral ischemia-reperfusion(CI-R).Methods:A total of 24 SD rats were randomized into sham-operation(n=6),model(n=6),EA(n=6)and EA PD 98059(n=6)groups.CI-R model was established by right middle cerebral artery occlusion(MCAO)for 2 hours and reperfusion for 24 hours.EA(disperse and dense waves,80-100 Hz,1-3 mA)was applied to "Dazhui"(GV 14)and "Baihui"(GV 20)for 60 minutes.The activity of extracellular signal-regulated kinases(ERK)positive cells in cerebral cortex tissue was detected with immunohistochemical method.Lumbar intrathecal injection of PD 98059,the inhibitor of mitogen activated protein kinase(MAPK)1(MEK1,2.78 mg/kg),was conducted in rats of EA PD 98059 group during CI-R.Results:In comparison with sham-operation group,the score of behavior test and the number of ERK immuno-reaction(IR)-positive neurons of model group decreased significantly(P<0.01,0.05),while compared with model group,the score and the number of ERK IR-positive neurons in EA group increased markedly(P<0.01).No significant difference was found between model group and EA PD 98059 group in behavior score and the number of ERK IR-positive neurons(P>0.05).Compared with sham-operation group,the mean area density and mean numerical density of ERK IR-positive neurons in model group were significantly lower(P<0.05),while in comparison with model group,the mean area density and mean numerical density in EA group were significantly higher(P<0.01);no significant differences were found between model and EA PD 98059 groups in the area density and numerical density(P>0.05).Conclusion:EA can reduce CI-R induced injury of cerebral neurons,which may be related to its effect in regulating ERK signaling pathway.