缓激肽对β淀粉样蛋白所致阿尔茨海默病动物模型行为学及形态学的影响

Effects of Bradykinin on β-Amyloid Protein-induced Alzheimer Disease Animal Model

目的观察缓激肽(BK)对β淀粉样蛋白(Aβ)所致阿尔茨海默病(AD)动物模型行为学及形态学的影响。方法20只健康Wistar大鼠,进行水迷宫训练后随机分为4组,在大鼠双侧海马背侧细胞带分别注入蒸馏水5μl(DW组),BK2.5μl、蒸馏水2.5μl(BK组),Aβ2.5μl、蒸馏水2.5μ(lAβ组),Aβ2.5μl、BK2.5μ(lAβ+BK组)。2周后观察各组大鼠水迷宫潜伏期值及海马、皮质区的HE和Nissl染色。结果Aβ+BK组大鼠水迷宫潜伏期明显延长,海马齿状回背侧细胞带明显受损或完全消失,CA1、CA4区细胞明显排列紊乱、数目减少,顶叶皮质神经元数目也有所减少;HE染色显示,齿状回背侧细胞带缺失区小胶质细胞明显增生。结论Aβ与BK同时注入大鼠海马可产生协同作用,提示可以用此方法建立AD动物模型。

Objective To observe the dysfunction of learning and memory and neuronal loss caused by bradykinin （BK） in normal mouse and Alzheimer disease （AD） model. Methods 20 rats were randomly divided into four groups. Distilled water （DW） 5 μl was injected into double hippocampal region in DW control group, BK 2.5 μl and DW 2.5 μl in BK injection group, β-Amyloid protein（ Aβ ） 2.5 μl and DW 2.5 μl in Aβ injection group,and BK 2.5 μl and Aβ 2.5 μl in co-injection BK with Aβ group. Long-term memory was examined 14 days after the administration. The sections were stained with haematoxylin-eosin （HE） and Nissl. Results Latent period of Aβ＋BK group was prolonged compared with other groups （P 〈 0.05 ）. The co-injection of Aβ with BK caused extensive neuronal loss not only around the injection site but also in distant areas. HE-stained showed microglia reaction around neuronal loss areas. Conclusion Co-injection of Aβ with BK can produce synergistic action and can be used to create a useful AD model.