电刺激小脑顶核对局灶脑缺血/再灌注后大鼠脑组织NF-кB、PPARγ、IкBα和COX-2mRNA表达的影响  

Effects of electrical stimulation to cerebellar fastigial nucleus on expressions of NF- кB, PPARγ, IкBα and COX-2 mRNA under cerebral ischemia/reperfusion in rats

作　　者：何兰英[1] 张蓓[1] 罗勇[2,3] 董为伟[2,3] 王咏龙[2,3] 

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

出　　处：《中国康复医学杂志》2014年第2期107-112,共6页Chinese Journal of Rehabilitation Medicine

摘　　要：目的:观察电刺激小脑顶核(FNS)对大鼠局灶脑缺血/再灌注(I/R)大脑缺血侧皮质PPARγ、IкBα和NF-кB P65蛋白表达的变化,以及对下游炎症因子COX-2 mRNA表达的影响,探讨FNS对大鼠局灶脑缺血/再灌注后脑保护作用的机制。方法:采用SD大鼠建立局灶I/R模型,随机分为6组。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),根据再灌注时间不同分为7d和14d两个亚组。采用免疫组织化学法检测NF-κB P65蛋白表达,分别采用Western blotting和逆转录—聚合酶链反应法(RT-PCR)检测PPARγ、IкBα蛋白和COX-2 mRNA表达,同时检测各组脑梗死体积。结果:免疫组织化学显示I/R 7d组和I/R 14d组NF-κB P65、PPARγ和IкBα蛋白较正常组显著增加(P<0.05),FNS组NF-κB P65蛋白表达显著低于相应I/R组(P<0.05),Western blotting检测显示FNS组PPARγ、IкBα蛋白表达明显高于相应正常组及I/R组(P<0.05),RT-PCR显示FNS组COX-2 mRNA表达较I/R组显著降低(P<0.05),而FNS组脑梗死体积较单纯I/R组明显减小(P<0.05)。结论:FNS可有效提高脑缺血/再灌注后PAARγ及IкBα表达,抑制由NF-κB P65调控的下游炎症因子COX-2mRNA的表达,减轻脑梗死体积,这可能是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（FNS） on expressions of NF-kB,PPARγ,IkBα and COX-2 mRNA in rats brain after cerebral ischemia/reperfusion（I/R）, and ex- plore the neuroprotection mechanism. Method： A focal cerebral I/R model was established by middle cerebral artery occlusion （MCAO）, and the rats were randomly divided into normal control group （NC group）, cerebral ischemia reperfusion group （I/R group）, I/R＋FNS group（FNS group）. Infarct volume was measured, the protein of NF-kB P65 in rats brain was detect- ed by immunohistochemistry, and the protein of PPARγ,IkBα was detected by Western blotting. The expres- sion of COX-2 mRNA was detected by RT-PCR. Result： Compared with NC group, the expressions of P65, PPARγ,IkBα protein and COX-2 mRNA increased under the I/R （P 〈 0.05）, FNS could effectively inhibit the expression levels of P65 protein and COX-2 mRNA （P〈 0.05）. FNS could effectively induce the expressions of PPARγ,IkBα protein （/9〈 0.05）, and reduce infarct volume significantly（P 〈 0.05）. Conclusion： FNS could effectively induce the expressions of PPARγ,IkBα protein, and effectively inhibit the expressions of P65 protein and COX-2 mRNA, and reduce infarct volume, which may be one of the mecha- nisms of its neuroprotective function on central nervous system.

关 键 词：电刺激 小脑顶核 NF-kB 脑缺血 再灌注 PPARΓ COX-2 IKBΑ 

分 类 号：R743.3[医药卫生—神经病学与精神病学]