电针对脑缺血再灌注模型大鼠纹状体NMDA受体NR2亚基蛋白表达的影响

Effect of electroacupuncture on protein expression of NMDA receptor subunits NR2 in corpus striatum of rats with cerebral ischemia reperfusion

目的观察脑缺血再灌注模型大鼠受损侧纹状体组织中NMDA受体调节亚单位NR2A和NR2B蛋白表达及其电针干预后的变化,探讨电针对缺血再灌注兴奋性氨基酸毒性的拮抗作用,进一步阐明电针治疗缺血性脑血管疾病的机制。方法用数字随机表将15只SD大鼠随机分成3组:假手术组、模型组、电针组,每组各5只。采用改良Longa线栓法制作大脑中动脉短暂性缺血再灌注模型,电针组大鼠在再灌同时电针"百会"、"大椎"两穴(连续波,频率3 Hz,电流强度1～3 mA),30 min,深度均为10 mm。免疫组织化学法及图像处理系统检测分析大鼠受损侧纹状体NR2A、NR2B蛋白表达情况。结果与假手术组相比,模型组大鼠纹状体组织中NR2A的表达量明显下降,而NR2B的表达量明显升高,给予电针"百会"、"大椎"穴后的大鼠纹状体组织NR2A表达细胞数及含量均明显高于模型组,表达NR2B的细胞数及含量均明显降低。结论电针可能通过激活NR2A受体蛋白表达,抑制NR2B受体蛋白的过量表达,从而调节NMDA受体复合物的整体功能活性,减少NMDA受体介导的兴奋性氨基酸毒性反应,减轻脑缺血再灌注引起的局灶性脑损伤,发挥一定的脑神经保护作用。

Objective To observe the effect of electroacupuncture （EA） on the protein expression of NMDA receptor snbunits NR2A and NR2B in corpus striatum of rats with cerebral ischemia-reperfusion （CI/R）, and explore the rivalry effect of EA on excitatory amino acids and molecular biology mechanism of the effect of EA. Methods 15 healthy male SD rats were randomized into sham, model and EA group （ n = 5）. CI/R model was established by right middle cerebral artery occlusion for 2 hours and reperfusion for 24 hours. EA （3 Hz, 1 - 3 mA） was applied to＂ Dazhui＂ （ GV 14） and＂ Baihui＂ （ GV 20） for 30 mimnutes. The expressions of NR2A and NR2B protein were detec ted by immunohistochemistry. Results Compared with sham group, the expression of NR2A was decreased and the expression of the NR2B was increased in corpus striatum of rats in model group. Compared with model group, the number of NR2A positive netirons in EA group was increased markedly （P 〈 0. 01 ） , the average grey scale of NR2A positive neurons in EA group was lower （P 〈 0. 05 ）, and the average opti- cal density in EA group were higher （P 〈 0.05 ）. The number and the average optical density of NR2B positive neurons in EA group was de- creased markedly （ P 〈 0, 05）, and the average grey scale of NP,2B positive neurons in EA group was higher （ P 〈 0. 05）. Conclusions EA treatment could increase the protein expression of NMDA receptor subunit NR2A, and decrease the protein expression of subunit NR2B, which indicates that EA treatment mav be a^ainst toxic effect nf excitatory amino acids relieve neural iniurv