电刺激小脑顶核对脑缺血再灌注后大鼠脑组织损伤的影响及其机制  

Effect of Electrical Stimulation to Cerebellar Fastigial Nucleus on Cerebral Ischemia-reperfusion Injury in Rats

作　　者：何兰英[1] 罗勇[2,3] 王健[1] 董为伟[2,3] 

机构地区：[1]成都市第二人民医院神经内科,四川成都市610017 [2]重庆医科大学附属第一医院神经内科,重庆市400016 [3]重庆市神经病学重点实验室,重庆市400016

出　　处：《中国康复理论与实践》2015年第9期1012-1015,共4页Chinese Journal of Rehabilitation Theory and Practice

摘　　要：目的探讨电刺激小脑顶核对大鼠局灶脑缺血再灌注后脑保护作用的机制。方法 Sprague-Dawley大鼠分为正常对照组(NC组)、缺血再灌注组(I/R组)、缺血再灌注后小脑顶核刺激组(FNS组)、毁损小脑顶核组(FNL组),后3组根据再灌注时间分为7 d和14 d两个亚组,每个亚组6只。大脑中动脉线栓法制作缺血再灌注模型。相应时间点采用Western blotting检测脑梗死周围组织核因子-κB(NF-κB)P50蛋白表达,逆转录-聚合酶链反应法(RT-PCR)检测肿瘤坏死因子-α(TNF-α)和Bcl-x L m RNA表达,同时检测各组脑梗死体积。结果与I/R组比较,FNS组NF-κB P50蛋白表达各时间点均增高(P<0.05),TNF-αm RNA表达明显降低(P<0.01),Bcl-x L m RNA表达升高(P<0.05),梗死面积明显减少(P<0.01)。与I/R组比较,FNL组上述指标均无显著性差异(P>0.05)。结论FNS可有效提高脑缺血再灌注后NF-κB P50蛋白、Bcl-x L m RNA表达,抑制下游炎症因子TNF-αm RNA的表达,减小脑梗死体积,可能是FNS发挥中枢神经保护的机制之一。Objective To investigate the effect of electrical stimulation to cerebellar fastigial nucleus on expression of nuclear factor-kappa B（NF-кB） P50, tumor necrosis factor-α（TNF-α） and Bcl-xL mRNA in rats brain after cerebral ischemia-reperfusion. Methods Sprague-Dawley rats were randomly divided into normal control group（NC group）, cerebral ischemia-reperfusion group（I/R group）, fastigial nucleus stimulation（FNS） group, and fastigial nucleus lesion（FNL） group. A focal cerebral ischemia-reperfusion model was established with middle cerebral artery occlusion（MCAO）. 7 and 14 days after operation, the infarct volume was measured, and the protein of NF-кB P50 in rats brain was detected with Western blotting; the expression of TNF-α and Bcl-xL mRNA was detected with RT-PCR. Results Compared with I/R group, the expression of NF- кB P50 protein increased in FNS group（P〈0.05）, with the decrease of expression of TNF- αmRNA（P〈0.01） and increase of Bcl-xL mRNA（P〈0.05）, while the infarct size decreased（P〈0.01）. There was no significant difference between FNL group and I/R group for all the measurements（P〉0.05）. Conclusion FNS could induce the expression of P50 protein and Bcl-xL mRNA, and inhibit the expression of TNF-α mRNA, and reduce infarct size, which may associated with the neuroprotection of central nervous system from injury.

关 键 词：脑缺血再灌注损伤 电刺激 小脑顶核 核因子-ΚB 肿瘤坏死因子-α BCL-XL 大鼠 

分 类 号：R743.3[医药卫生—神经病学与精神病学]