Alzheimer病铝中毒大鼠模型海马结构中β-APP和GFAP研究

Study About GFAP and β-APP in Hippocamp of the Aluminium Treated Rat Models of Alzheimer Disease

目的 通过用氯化铝灌胃建立的Alzheimer病 (AD)动物模型 ,探讨AD发病中星形胶质细胞增生和 β -淀粉样蛋白前体 (β -APP)的表达及可能的联系。 方法 应用免疫组化方法观察AD动物模型中海马各区胶质原纤维酸性蛋白 (GFAP)和 β-APP表达情况。 结果 (1)GFAP免疫组化标记可见动物模型海马各区星形胶质细胞明显增生 (P <0 .0 1) ,且增生细胞在CA2和CA3区最明显。 (2 ) β -APP免疫组化标记见动物模型海马各区内 β -APP阳性细胞明显增多 (P <0 .0 1) ,以CA2和CA3区最为明显。结论 星形胶质细胞增生在AD发病早期即起作用 ,与 β-APP过表达有密切关系。

Objective To establish the Alzheimer disease (AD) rat model through pretreatment with aluminium chloride to investigate the possible etiopathology of AD. Methods After pretreatment with aluiminium chloride,the model of demential was established.The AD animal models were concluded to be successful or not through the performance of Y-shape maze task.With the immunohischemical method of ABC,we observed the proliferation of astrocytes and the expression of β-APP in the hippocampal formation of rat. Results (1)More astrocytosis was found in hippocampal formation in the animal models than that in the controls( P < 0.01 ). The astrocytes were the most in CA2 and CA3 regions of hippocampal formation.(2)More β-APP-positive immunoreactive (β-APP +) neurocytes were found in hippocamapal formation in the animal models than that in the controls( P < 0.01 ). β-APP + neurocytes were the most in CA2 and CA3 regions of hippocampal formation.Conclusion The astrocytosis may be related with the overexpressin of β-APP and may be a major factor in AD onset.