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背景:预先电刺激小脑顶核(fastigialnucleus,FN)具有明确的缺血脑保护作用,但其机制尚不十分清楚。研究缺血诱导的蛋白激酶C(proteinkinaseC,PKC)同工酶γ,δ异常表达,可使人们从新的角度去认识和探索预先电刺激FN缺血脑保护作用的机制。目的:观察预刺激脑缺血大鼠小脑顶核不同时相PKC同工酶γ,δ蛋白表达。设计:随机对照实验。地点和对象:实验地点:重庆医科大学神经病学研究所。Wistar雄性大鼠48只,随机将动物分为单纯缺血再灌注组(I/R),假手术组(I/R’),刺激小脑齿状核(dentatenucleus,DN)I/R组(I/RDN),刺激小脑FNI/R组(I/RFN);其中I/RDN,I/RFN又分别分为3组:缺血前1,4,7d刺激。每组动物为6只。干预:采用线栓法大鼠大脑中动脉栓塞再灌注模型,缺血时间均为1.5h再灌注24h;于缺血前1,4,7d分别刺激小脑顶核、齿状核1h。主要观察指标:以尾状核冠状切面作为观察对象,应用免疫组织化学方法观察对照组、假手术组、刺激小脑顶核组和齿状核组PKCγ,δ的表达情况。结果:缺血前1,4,7d刺激小脑齿状核各组、单纯缺血再灌注组、假手术组PKCγ,δ阳性细胞数比较无显著性差异(P>0.05),而缺血前1,4,7d预刺激小脑顶核能明显抑制PKCγ,δ蛋白的表达(t=2.372～6.632,P<0.05)。结论:缺血性脑损害能诱导PKCγ,δ蛋白表达上调,?
BACKGROUND: Pre-electrical stimulation of fastigial nucleus (FN) has a clear ischemic brain protective effect, but its mechanism is not well understood. Studying ischemia-induced aberrant expression of protein kinase C (PKC) isozymes, δ, δ may allow us to recognize and explore the mechanism of pre-electrical stimulation of cerebral ischemia-reperfusion injury in FN. OBJECTIVE: To observe the expression of PKC isoenzyme γ, δ protein in different phases of cerebellar fastigial nucleus in pre-stimulated rats. Design: Randomized controlled experiment. Location and Subjects: Experimental Location: Institute of Neurology, Chongqing Medical University. Forty - eight Wistar male rats were randomly divided into three groups: I / R group, sham operation group (I / R ’), denture nucleus I / R group (I / RDN) to stimulate the cerebellar FNI / R group (I / RFN). I / RDN and I / RFN were further divided into three groups: 1, 4 and 7 days before ischemia. 6 animals in each group. Intervention: The middle cerebral artery occlusion (MCAO) reperfusion model was adopted. The ischemia time was 1.5h and then reperfusion 24h. The apical nucleus and dentate nucleus of cerebellum were stimulated at 1, 4 and 7 days before ischemia respectively. MAIN OUTCOME MEASURES: Coronal section of the caudate nucleus was used as observation object. Immunohistochemistry was used to observe the expression of PKCγ and δ in the control group, sham operation group, fastigial nucleus pulposus group and odontoid nucleus group. Results: There was no significant difference in the number of positive cells of PKCγ and δ between sham-operated group and ischemia-reperfusion group (P> 0.05) The preconditioning of cerebellar fastigial nucleus significantly inhibited the expression of PKCγ and δ (t = 2.372 ~ 6.632, P <0.05) at 4 and 7 days. Conclusion: Ischemic brain damage can induce the up-regulation of PKCγ and δ protein expression.