电针预处理对大鼠脑缺血再灌注损伤后EAAT2的表达研究

目的研究电针预处理对脑缺血再灌注损伤后大鼠缺血半暗带兴奋性谷氨酸转运体2(EAAT2)表达的影响,探讨EAAT2在电针预处理诱导脑缺血耐受中的作用。方法 18只SD雄性大鼠随机分为3组(n=6):分别为假手术(Sham)组、右侧大脑中动脉阻闭(MCAO)组、电针预处理(EA)组。假手术组仅分离血管,不进行阻闭,术后24 h检测;MCAO组用MCAO法致缺血120 min后于再灌注24 h检测;EA组大鼠予电针刺激30 min,刺激结束2 h后处理同MCAO组。3组大鼠在观察神经行为学变化后取材,通过2,3,5-氯化三苯四唑(TTC)染色评估梗死面积,并检测EAAT2 mRNA及蛋白表达水平。结果电针预处理能明显降低脑梗死容积百分比(P0.01),提高MCAO大鼠神经行为学评分,诱导脑缺血耐受并抑制脑缺血再灌注损伤后24 h EAAT2表达的下降(P0.01)。结论脑缺血再灌注损伤后,EAAT2表达下降,而电针预处理能显著抑制缺血半暗带EAAT2的表达下调,诱导脑缺血耐受,从而减轻脑缺血再灌注损伤。

Electroacupuncture preconditioning protects rats against cerebral ischemia reperfusion injury via EAAT2

Objective The effect of electroacupuncture preconditioning on the expression of excitatory amino acid transporter 2 （EAAT2） in the rat brain following transient focal cerebral ischemia is investigated and the role of EAAT 2 in the electroacupuncture （EA） preconditioning induced ischemic tolerance in rats is explored.Methods Eighteen rats were assigned to three groups （with 6 rats in each group）：sham group,middle cerebral artery occlusion （MCAO） group and electro-acupuncture preconditioning （EA） group.In sham group the blood vessels were separated and no occlusion was performed; the rats in MCAO group were treated by middle cerebral artery occlusion of the right side for 120 min following 24 h reperfusion; the rats in the EA group were performed electroacupuncture for 30 min and then received the same treatment as the MCAO group 2 h later.After the neurological functions were observed,the rats were killed.The infarct volume was determined by 2,3,5-triphenyl-2H-tetrazolium chloride （TTC） staining.The level of EAAT2 in the ischemic penumbra was investigated by Western blot and qRT-PCR.Results The neurological behavior scores were better in EA group than in MCAO group,and the infarct volumes in EA group were significantly smaller than those in MCAO group （P 〈0.01）.The down-regulated expression of EAAT2 was suppressed by EA preconditioning （P 〈0.01）.Conclusion EA preconditioning has a significant neuroprotective effect via suppressing the down-regulation of EAAT2 after ischemia reperfusion.