针刺调节MAPK/ERK通路对脑缺血模型大鼠的干预作用

Research of Intervention with Electroacupuncture Through Regulating MAPK/ERK Pathway for Cerebral Ischemia Rats

【目的】观察电针调节丝裂原活化蛋白激酶/细胞外信号调节激酶(MAPK/ERK)通路对脑缺血模型大鼠的干预作用。【方法】选用SD大鼠,随机分为假手术组、模型组和电针组,每组又分为2 h、1 d、3 d 3个亚组,后2组采用热凝闭大脑中动脉法复制局灶性脑缺血模型。电针组针刺百会、大椎穴,每天1次,分别治疗2 h、1 d、3 d。每组均进行神经行为学评分及Y迷宫测试,并采用免疫组化法检测脑组织CA1区、CA3区磷酸化EPK(p-EPK)阳性细胞表达的积分光密度值总和(Dsum)。【结果】模型组大鼠神经行为学评分显著升高、Y迷宫测试时间显著延长(均P<0.01),电针1 d、3 d组可显著降低神经行为学评分,缩短Y迷宫测试时间,与模型组及电针2 h组比较差异均有显著性意义(P<0.05或P<0.01)。假手术组无p-EPK阳性细胞表达,模型组CA1区和CA3区Dsum显著升高(均P<0.01),电针各组CA1区、CA3区Dsum均较模型组显著降低(P<0.05或P<0.01),而电针1 d、3 d组Dsum降低幅度显著大于电针2 h组(均P<0.05)。【结论】电针可以通过调节MAPK/ERK通路,降低p-ERK在脑缺血早期的表达,从而改善脑缺血模型大鼠的脑组织损伤。

Objective To observe the intervention with electroacupuncture （EA） through regulating protein kinase （MAPK/ERK） pathway for cerebral isehemia rats. Methods SD rats were randomized into pseudo- operation group, model group and EA group. And the three groups were divided into 2-hour, one-day and 3-day subgroups according to the observation time. Focal cerebral ischemia （FCI） rat models were established by middle cerebral artery occlusion （MCAO） with heat-coagulation method. EA group received EA on Baihui （GV20） and Dazhui （ GV14）, qd, for 2 hours, one day and 3 days respectively. The learning and memory abilities of the rats in Y maze test and their neuroethological score were observed. Immunohistochemical method was used to observe the expression of phosphorylated extracellular signal-regulated kinase （p-ERK） after ischemia in CA1 area and CA3 area. Results In the model group, the neuroethological score was markedly increased, time for arriving the safe area in Y maze was prolonged （ P 〈 0. 01 compared with those in the pseudooperation group） , EA for one day and 3 days counteracted the above changes, and the difference was significant as compared with the model group and the group of EA for 2h （P 〈 0.05 or P 〈 0.01 ）. Pseudo-operation group had no cells with positive p-ERK expression, the model group had a higher total score of p-ERK optical density in CA1 area and CA3 area （ P 〈0. 01 ） , and EA decreased the total score of p-ERK optical density （ P 〈0.05 or P 〈 0. 01 compared with the model group） , the decrease being obvious in the group of EA for one day and 3 days （P 〈 0. 05 compared with the group of EA for 2h）. Conclusion EA can relieve the cerebral injury in cerebral ischemia rats through regulating MAPK/ERK pathway and by decreasing p-ERK expression in the early stage of cerebral ischemia.