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目的 通过海马注射缓激肽复制阿尔茨海默病神经原纤维变性大鼠模型。方法 采用脑立体定位注射技术向海马注射缓激肽 (bradykinin ,BK) ,在整体水平上调钙 /钙调素依赖性蛋白激酶 Ⅱ (CaMK Ⅱ )活性 ;电跳台法测试大鼠学习与记忆状况 ;免疫组化技术检测tau蛋白质磷酸化状况。结果 注射BK模型鼠组海马区特定位点磷酸化的tau(12E8、M4和PHF 1)其显色均强于对照组 ,模型组鼠特定位点未磷酸化的tau(tau 1)显色弱于对照组 ,并导致模型组大鼠学习记忆障碍。BK模型鼠与对照鼠出现错误次数分别为 8.3± 2 .5和 6 .9± 3.1(P <0 .0 5 ) ,受电击时间为 (73 .6± 2 5 .1)s和(35 .8± 2 3.7)s(P <0 .0 1)。结论 BK可在整体水平造成骨架蛋白tau的过度磷酸化和大鼠学习与记忆功能障碍。为复制具有AD行为及病理特征的动物模型奠定了基础。
OBJECTIVE: To replicate the Alzheimer’s disease rat model of neurofibrosis by injecting bradykinin into the hippocampus. Methods Bradykinin (BK) was injected into hippocampus by stereotaxic injection and the activity of CaMK Ⅱ was up-regulated. The learning and memory status of rats was tested by electroporation. Immunohistochemistry was used to detect phosphorylation of tau protein. Results The phosphorylation of tau (12E8, M4 and PHF1) at specific sites in hippocampus of BK model rats was stronger than that of control group. The unphosphorylated tau (tau 1) In control group, and caused learning and memory impairment in model group rats. The number of errors in BK model rats and control mice were 8.3 ± 2.5 and 6.9 ± 3.1, respectively (P <0.05), and the durations of shock were (73.6 ± 2.51) s and 8 ± 2 3.7) s (P <0.01). Conclusion BK can cause over-phosphorylation of scaffold protein tau and dysfunction of learning and memory in rats as a whole. Which laid the foundation for the replication of animal models with AD behavior and pathological features.