缓激肽对β-淀粉样蛋白所致阿尔茨海默病动物模型脑中Tau蛋白磷酸化的影响  

Effects of Bradykinin on Tau phosphorylation in β-Amyloid Protein-induced Alzheimer Disease

作　　者：张文珺 彭方南[2] 商秀丽[3] 

机构地区：[1]东营市人民医院神经内科,东营257000 [2]东营市胜利油田中心医院神经内科 [3]中国医科大学附属第一医院神经内科

出　　处：《滨州医学院学报》2012年第6期423-425,共3页Journal of Binzhou Medical University

摘　　要：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)动物模型脑中Tau蛋白磷酸化的影响。方法随机选取20只健康Wister大鼠,进行水迷宫训练后分为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、DW2.5μl(BK组),Aβ2.5μl、DW2.5μl(Aβ组),Aβ2.5μl、BK2.5μl(Aβ+BK组)。2周后观察各组大鼠海马、皮层区的磷酸化Tau阳性细胞数。结果 Aβ+BK组海马CA1、CA4区及皮层区磷酸化Tau蛋白免疫阳性细胞积分光密度值明显高于其他各组。结论 Aβ与BK同时注入大鼠海马可产生协同作用,引起Tau蛋白更明显的磷酸化,提示可以用此方法建立AD动物模型。Objective To observe the Tau phosphorylation caused by bradykinin（BK ） in normal mouse with Alzheimer Disease （AD）. Methods Twenty rats were randomly divided into four groups. Distilled water （DW） 5μl was injected into double hippoeampal region in DW control group,BK 2. 5 μl and DW 2. 5 μl in BK 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. The Tau deposition was detected 14 days after the administration. Results The integrated OD total of Tau positive cell was significantly higher in co-injection of BK with Aβ group than others. Conclusion Aβ and BK injected simultaneously into hippoeampus of rats would work synergistically to cause more obvious phosphorylation of Tau protein and we could use this method to establish an animal model.

关 键 词：缓激肽 Β-淀粉样蛋白 阿尔茨海默病 磷酸化TAU蛋白 

分 类 号：R393[医药卫生—基础医学]