电项针对全脑缺血VD模型大鼠PI3K/AKT/GSK-3β信号通路的影响

Effect of electroacupuncture at neck points on PI3K/AKT/GSK-3β signal pathway in the model rats of cerebral ischemic vascular dementia

目的研究电项针对全脑缺血血管性痴呆(vascular dementia,VD)模型大鼠磷脂酰肌醇-3-激酶/丝氨酸-苏氨酸蛋白激酶/糖原合成酶激酶-3β(Phosphatidylinositol-3 kinase/serine-threonine kinase/glycogen synthase kinase-3β,P13K/AKT/GSK-3β)信号通路的影响。方法采用四血管阻断方法制备VD模型大鼠,电项针组取双侧风池穴、供血穴,电针30 min/次,1次/d,治疗14d。采用Y迷宫评价大鼠学习记忆能力;荧光定量PCR(RT-PCR)、Western blot法检测大鼠海马组织中磷酸化蛋白激酶B(phosphorylatedproteinkinaseB,p-AKT)、磷酸化糖原合成酶激酶-3β(Phosphorylated GSK-3β,P-GSK-3β)mRNA和p-AKT、p-GSK-3β蛋白的表达。结果与模型组比较,电项针组可显著提高VD大鼠Y迷宫学习与记忆正确次数(P<0.01)。与模型组比较,电项针组大鼠海马组织中p-AKT、p-GSK-3βmRNA和p-AKT、p-GSK-3β蛋白表达均有不同程度的升高(P<0.01)。结论电项针能够改善VD模型大鼠学习记忆能力,具体机制可能是激活PI3K/AKT/GSK-3β信号通路,发挥抗凋亡作用,起到对缺血海马神经元的保护作用。

Objective To study the effect of electroacupuncture（ EA） at neck points on Phosphatidylinositol-3 kinase/serine-threonine kinase/glycogen synthase kinase-3β（ PI3K/AKT/GSK-3β） signal pathway in the model rats of cerebral ischemic vascular dementia（ VD）. Methods The four-vessel occlusion method was adopted to prepare VD model rats. In the EA group,EA at neck points was used at bilateral Fengchi（ GB20） and Gongxue（ Extra）,30 min each time,once a day,for 14 days. The Y maze method was provided to evaluate the learning and memory ability of the rats. RT-PCR and Western blot were adopted to determine the expressions of p-AKT,P-GSK-3β mRNA as well as p-AKT and p-GSK-3β protein in the hippocampal tissue. Results Compared with the model group,the correct frequencies of learning and memory in the Y maze test were increased significantly in the EA group（ P 0. 01）. Compared with the model group,the expressions of p-AKT,P-GSK-3β mRNA as well as p-AKT and p-GSK-3β protein in the hippocampal tissue were increased to different degrees in the EA group（ P 0. 01）. Conclusion EA at neck points improves the learning and memory ability of VD model rats. The effects are possibly achieved through activating PI3 K/AKT/GSK-3β signal pathway,giving the play to anti-apoptosis and protecting ischemic hippocampal neurons.