中文摘要：

目的 观察Wistar大鼠局灶脑缺血／再灌注后，脑内核因子—κB（NF—κB）活性及其活化的基本规律，并探讨电刺激小脑顶核（FNS）对其影响。方法成年雄性Wistar大鼠27只，随机分为正常组、单纯局灶脑缺血／再灌注组（模型组）和局灶脑缺血／再灌注＋电刺激小脑顶核治疗组（FNS治疗组）。采用线栓法制备右侧大脑中动脉闭塞（MCAO）模型，缺血时间均为2h，根据再灌注时间分为缺血2h／再灌注3，6，12和24h组？模型组不给予任何干预处理，FNS治疗组在缺血2h再灌注即刻给予FNS治疗1h。用Westernblot法检测缺血脑组织核抽提物中NF—κBp65蛋白的表达，用电泳迁移率改变分析法（EMSA）检测核抽提物中NF—κBDNA的结合活性=结果正常组大鼠脑组织核抽提物中有少量NF—κBp65蛋白，NF—κBDNA结合活性较弱。模型组再灌注各时间点，即再灌注3，6，12和24h，NF—κBp65蛋白含量均高于正常组，其中再灌注6h和12h均显著高于正常组（P〈0．05）。模型组NF—κBp65蛋白含量变化趋势为：再灌注3h〈再灌注6h〈再灌注12h，再灌注12h达峰值，各组间差异具有统计学意义（P〈0．05）；再灌注24h时NF—κBp65蛋白含量明显低于再灌注6h和12h（P〈0．05）。模型组NF—κBDNA结合活性除再灌注3h外，其余3个时间点均显著高于正常组（P〈0．05）；模型组再灌注3h时，NF—κBDNA结合活性明显弱于组内其余3个时间点（P〈0．05），这3个时间点均为高活性状态，组内差异无统计学意义（P〉0．05）。FNS治疗组NF—κBp65蛋白含量及NF—κBDNA结合活性的变化趋势与模型组相似。其中，再灌注6h和12h时，FNS治疗组NF—κBp65蛋白含量明显低于模型组相应时间点（P〈0．05）；再灌注6，12和24h时，FNS治疗组NF—κBDNA结合活性也明显低于模型组相应时间点（P〈0．05）。结论大鼠局灶脑缺血／再灌注后缺血脑组

英文摘要：

Objective To explore changes in the activation and activity of nuclear factor kappa B（ NF κB） after cerebral ischemia-reperfusion （CIR） in rats, and to investigate the effects of electrostimulation of the fastigial nucleus （FNS） on these indicators. Methods Twenty-seven adult male Wistar rats were randomly divided into three groups： a normal control group （n=3）, a CIR group （n=12） and a CIR＋ FNSgroup （n=12）. Middle cerebral artery obturation （MCAO） was established by suturing the right MCA, and the treated rats were then randomly divided into four subgroups reperfused for 3 h,6 h,12 h and 24 h. FNS was administrated to the CIR ＋ FNS groups at 2 h after CIR for 1 h, while there was no treatment of the CIR group. Then the expression of NF κB p65 protein in nuclear extracts was detected using western blotting, and the DNA binding activity of NF κB was measured by electrophoretic mobility shift assay （EMSA）. Results NF κB p65 protein concentrations in the nuclear extracts were increased at the different reperfusion time points, especially at 6 h and 12 h （P 〈 0.05 ）compared with the normal control group. NF κB DNA binding activities were also significantly improved at 6 h, 12 h and 24 h （P 〈 0.05）. Compared with the CIR group, the levels of NF κB p65 protein in the CIR ＋ FNS group were distinctly decreased at 6 h and 12 h after reperfusion （P 〈 0.05 ）, while the NF κB DNA binding activities were obviously decreased at 6 h, 12 h and 24 h （P 〈0.05）. Conclusions The expression of NF κB protein and NF κB DNA binding activity can be inhibited by FNS, which might be one of the mechanisms of the anti-inflammatory effects of FNS.