论文部分内容阅读
目的 :观察预刺激脑缺血大鼠小脑顶核不同时相蛋白激酶C同工酶γ、δ蛋白表达。方法 :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 .5hr/再灌注 2 4hr;于缺血前1、4、7天分别刺激小脑顶核、齿状核 1hr。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单纯缺血 /再灌注组、假手术组、刺激小脑顶核组和刺激齿状核组PKCγ、δ的表达情况。结果 :缺血前 1、4、7天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 .0 5) ,而缺血前 1、4、7天预刺激小脑顶核能明显抑制PKCγ、δ蛋白的表达(P <0 .0 5)。结论 :缺血性脑损害能诱导PKCγ、δ蛋白表达上调 ,预先电刺激小脑顶核的缺血脑保护作用可能与其下调PKCγ、δ蛋白表达有关
Objective: To observe the expression of protein kinase C isoenzyme γ and δ in cerebellar fastigial nucleus in preconditioning ischemic rats. Methods: The middle cerebral artery occlusion / reperfusion model was induced by thread occlusion. The ischemia time was 1.5 hr / reperfusion for 24 hr. The maxillary nucleus and dentate nucleus were stimulated at 1, 4 and 7 days before ischemia 1hr. The coronal section of the caudate nucleus was taken as the observation object. Immunohistochemistry was used to observe the expression of PKCγ, δ in the ischemia / reperfusion group, the sham operation group, the fastigial nucleus pulposus group and the dentate gyrus group. Results: There was no significant difference in the number of positive cells of PKCγ and δ in the sham-operation group after stimulating the cerebellar dentate gyrus in each group on the 1st, 4th and 7th days before ischemia and in the ischemia / reperfusion group only (P> 0.05) Preconditioning of cerebellar fastigial nucleus 1, 4 and 7 days before ischemia significantly inhibited the expression of PKCγ and δ proteins (P <0.05). CONCLUSION: Ischemic brain damage can induce the upregulation of PKCγ and δ proteins. Preconditioning electrical stimulation of the cerebellar fastigial nucleus may be related to the downregulation of PKCγ and δ protein expression