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 investigate whether electrical fore stimulation of cerebellar fastigial nucleus(FN) could influence changes of cerebral PKC γ and PKC δ expression in cerebral ischemia reperfusion (I R) rats . Methods: 48 Wistar rats were randomly divided into I R group

sham operation group

DN stimulation (S) group and FN S group

and each of the later two groups were further divided into 3 groups according to fore stimulation duration (one day

4 days and 7 days). The middle cerebral artery occlusion and reperfusion(MCAo R) model was performed in Wistar rats using intraluminal cauterized catgut ball blocking method. Cerebellar FN and DN (Dentate Nucleus) were stimulated electrically for 1 hr

one day

4 days and 7 days before MCAo R(1.5 hr/24 hr). PKC γ

PKC δ protein expression was determined with immunohistochemical staining technique. Results: PKCγ and δ positive reaction cells distributed in cerebral cortex

hippocampus and the ischemic half shadow area. There were no significant differences among I R group

sham operation group

DN stimulation (S) subgroups (1 day

4 days and 7 days) in PKCγ and δ positive cell counts (P>0.05)

but in comparison with DN stimulation subgroups

the positive cells in FN stimulation subgroups were significantly fewer (P<0.01)

which even lasted 7 days (P<0.05). Conclusion: Cerebral ischemia can induce abnormal expression of PKC γ and PKC δ

and FN fore stimulation generated down regulation of PKCγ and δ expression may contribute to its protective effect on cerebral ischemia.