β-淀粉样蛋白对AD大鼠脑内胶质细胞的影响作用研究

Ultrastructural changes of neurogliocytes after amyloid-beta protein injected into Meynert nucleus in AD rats

目的 探讨Meynert核注射 β 淀粉样蛋白 (Aβ)后对大鼠脑神经胶质细胞超微结构的影响及其可能机制。方法 将 1μLAB1-40 (10 μg/ μL)在立体定向仪下注入大鼠右侧Meynert核 ,分别于 1周、4周时用透射电镜观察脑组织中神经胶质细胞超微结构变化。结果 实验组Meynert核、海马区和皮层区均可见神经胶质细胞增生 ,其中以小胶质细胞为主 ,星形胶质细胞次之 ;小胶质细胞聚集并吞噬变性神经细胞以及血管周围可见增生活跃的小胶质细胞聚集 ;神经元胞体皱缩 ,胞浆浓缩 ,核染色质固缩成团块状并见边聚现象 ,核膜尚完整 ,有发生凋亡的趋势 ;正常对照组和假手术组无上述变化。结论 Aβ能引发CNS神经胶质细胞增生并活化 ,免疫炎性反应在AD记忆障碍和痴呆形成过程中可能具有重要作用。

Objective To investigate the ultrastructural changes of neurogliocytes after amyloid beta protein injected into Meynert nucleus in rats.Methods Aβ 1-40 (10 μg) was microinjected into the right Meynert nucleus of rats, 1 week and 4 weeks later, ultrastructure of neurogliocyte was observed under transmission electron microscopy(TEM).Results In experimental group, the TEM examination revealed neurogliocyte hyperplasia reactively in the Meynert nucleus, hippocampus, cortex subfields, especially microglia, then asytrocyte. Microglia assembled and licked up degenerative neurons. Activated microglia masses were observed near blood vessel. Neuron cell bodies became shrunken, whereas the chromatins were condensed, compact patches like crescent moons with condensed nuclear chromatin but with no apparent nuclear membrane disruption. No change could be seen in control groups.Conclusions The result of this study indicated that Aβ could induce the neurogliocyte hyperplasia and activated. Immunoinflammation in brain might play an important role for memory disorder and AD formation.