trkA和Aβ-与阿尔茨海默病大鼠发病机制的关系.docVIP

　　trkA和Aβ1-40与阿尔茨海默病大鼠发病机制的关系 【摘要】 目的 采用穹隆-海马伞切断及双侧卵巢切除的方法制作阿尔茨海默病（Alzheimer,disease AD）模型，观察AD模型大鼠脑内皮层区、海马CA1区、杏仁复合体区和Meynert核区酪氨酸激酶原癌基因（tyrosine kinase proto-onco-geneA,TrkA）和β淀粉样肽1-40（Amyliod β1-40）的表达与对照组比较有何变化，以探讨二者的变化与AD发病机制的关系。方法 取健康雌性eynert核区等部位trkA和Aβ1-40阳性细胞的表达与对照组比较是否不同。结果 对照组大鼠脑内的各观察区内Aβ1-40只有少量表达，trkA表达无明显改变；AD模型组大鼠脑内的皮层区、海马CA1区、杏仁复合体区和基底前脑Meynert核区Aβ1-40表达显著增多（Plt;0.05），各模型组zhijian 相互比较，Aβ1-40的表达无明显差异（Pgt;0.05）；AD模型组大鼠脑内的皮层区、海马CA1区、杏仁复合体区和基底前脑Meynert核区trkA的阳性细胞显著减少（Plt;0.05），各模型组之间相互比较，穹隆海马伞切断加卵巢切除组较穹隆海马伞切断组和卵巢切除组trkA减少显著（Plt;0.05），穹隆海马伞切断组与卵巢切除组之间trkA表达差异无显著性（Pgt;0.05）。结论 AD模型组大鼠脑内皮层区、海马CA1区、杏仁复合体区和基底前脑Meynert核区内Aβ1-40的阳性细胞显著增加，而trkA的阳性细胞显著减少，提示Aβ1-40的表达增多和trkA的表达减少可能与老年性痴呆发病机制相关，可能是临床AD发病的病理基础。 【关键词】 穹隆-海马伞切断；卵巢切除；酪氨酸原癌基因；β淀粉样肽1-40；大鼠；阿尔茨海默病 【Abstract】 Objective To observe the expression of trkA and Aβ1-40 in the different areas of the brain bria/fornix ake AD model and discuss the relationship of trkA and Aβ1-40 ale rats ly and equally divided into control group, fimbria/fornix transection and ovariectomized group, ovariectomized group and fimbria/fornix transaction group. The bilateral fimbria-fornix of brain bria/fornix transaction group. The bilateral ovaries of rats ized group. In the fimbria/fornix transection and ovariectomized group, bilateral fimbria-fornix of brain eanake simulational model of AD. Immunoreactive cell of trkA and Aβ1-40munohistochemical munoreactive cell of trkA and Aβ1-40 in the cerebral cortex, hippocampus CA1, Meynert nucleus and almond complex ber of masculine cell es microscope randomly selected 5 fields in every detected area, and then the average number of trkA and Aβ1-40 in one field in normal group odel groups pared respectively in model groups. Firstly the numbers arkably increased in the cortex, hippocampus CA1, Meynert nucleus and almond complex of the brain in the AD model groups as compared to that in the normal group (Plt;0.01). Hoodel groups (Pgt;0.05). As compared to the normal group, the expression of trk