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机构地区:[1]青岛大学医学院病理生理学教研室,山东青岛266021
出 处:《齐鲁医学杂志》2007年第2期120-121,125,共3页Medical Journal of Qilu
摘 要:目的了解蛋白激酶与蛋白磷酸酯酶活性改变对阿尔茨海默病(AD)样神经原纤维变性的影响。方法选择SD大鼠24只,随机分为实验组和对照组,各12只。实验组采用脑立体定位注射技术,向海马区注射20 mmol/L缓激肽(BK)和4.2 mmol/L环孢菌素A(CSA)各0.2 mL,对照组注射人工脑脊液0.4 mL,电跳台法测试大鼠学习与记忆状况;免疫印迹法检测Tau蛋白质磷酸化状况。结果实验组鼠出现错误次数多于对照组(t=3.362,P<0.01),受电击时间长于对照组(t=4.537,P<0.01)。实验组海马区12E8显色强于对照组,Tau-1显色弱于对照组。结论BK和CSA可诱发Tau蛋白多个位点出现AD样异常磷酸化,导致动物学习记忆障碍。Objective To study the effects of protein kinase and protein phosphatase imbalance on Alzheimer-like phosphorylation of Tau and abnormal behavior in rats. Methods BK and CSA or CSF were injected into hippocampus, and their behaviors by electronic attack-jump experiment and phosphorylation of Tau were observed by immunostaining assay. Results An obvious disturbance in learning and memory was seen with BK and CSA injected rats. The results obtained by immunostaining assay indicated that the staining for 12E8 was stronger, and for Tau-1 or PHF-1 were weaker in BK and CSA injected rats compared with control group. The BK arid CSA injected rats showed obvious deficits in behavior (t=3. 362, P〈0.01). The rats were more struck by lightening than the controls (t=4. 537, P〈0.01). Conclusion BK and CSA can induce both Alzheimer-like Tau phosphorylation and behavioral disturbance.
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