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采用ＡｌＣｌ３诱导，建立Ａｌｚｈｅｉｍｅｒ病（ＡＤ）模型大鼠。用维生素Ｅ（ＶＥ）（５ｍｇ／１００ｇ体重·ｄ－１）对ＡＤ模型大鼠进行灌胃治疗。通过行为测试，光镜形态学观察，用免疫细胞化学ＡＢＣ结合图像定量分析的方法，对ＡＤ大鼠行为改变，海马结构ＣＡ１区淀粉样蛋白免疫反应阳性神经元的形态和数目、胞体平均截面积和光密度以及β淀粉样蛋白的沉积变化进行观察。结果显示ＶＥ组大鼠治疗３个月和５个月后，受电击次数和潜伏期较对照组明显减少和延长（Ｐ＜００１），３个月与５个月之间有显著性差异（Ｐ＜００１）；ＶＥ组大鼠海马结构ＣＡ１区淀粉样蛋白免疫反应阳性神经元的形态和数目、胞体平均截面积和光密度值，３个月和５个月较对照组均有明显减少和降低（Ｐ＜００１），３个月和５个月之间也有显著性差异（Ｐ＜００１），β淀粉样蛋白样反应染色减少或消失。说明ＶＥ可以改善ＡＤ模型大鼠的学习记忆，其作用机制是通过抑制和清除海马结构ＣＡ１区β淀粉样蛋白的沉积来实现的，作用效果随治疗时间的延长而更加明显。本实验研究结果为临床应用ＶＥ治疗老年性痴呆提供了形态学依据。
The Alzheimer’s disease (AD) model rats were established by AlCl3 induction. AD model rats were gavaged with vitamin E (VE) (5 mg / 100 g body weight · d-1). The behavioral changes, the morphology and number of amyloid-immunoreactive neurons in hippocampal CA1 area of hippocampus, the average cross-sectional area of cell body And optical density and deposition of β-amyloid changes were observed. The results showed that the rats in VE group were significantly reduced and prolonged (P <001) after 3 and 5 months of treatment, compared with the control group, and there was significant difference between 3 and 5 months (P < P <001). The morphology and number of amyloid-immunoreactive neurons in hippocampal CA1 area of rats in VE group were significantly lower than those in control group at 3 and 5 months And decreased (P <001). There was also a significant difference between 3 and 5 months (P <001). The staining of β-amyloid-like reaction decreased or disappeared. These results suggest that VE can improve the learning and memory of AD model rats. Its mechanism is through inhibiting and eliminating the deposition of β-amyloid in the CA1 region of hippocampal formation, and the effect is more obvious with the prolongation of treatment time. The experimental results provide a morphological basis for the clinical application of VE in the treatment of senile dementia.