【摘要】 目的采用β-淀粉样蛋白(β-amyloid,Aβ)25-35注射法建立Alzheimer病(Alzheimer disease,AD)大鼠模型,观察该AD模型中tau蛋白和微管相关蛋白2(microtubule-associated protein-2,MAP2)表达情况。方法将健康雄性Wistar大鼠随机分成健康对照组、假手术组及AD模型组,以凝聚状态的Aβ25-35经大鼠右侧海马注射制作AD模型,造模2周后应用HE染色和免疫组化方法,观察AD模型鼠脑中海马CA1区病理形态以及tau蛋白和MAP2的表达。结果AD模型组大鼠海马CA1区锥体细胞层紊乱、变稀、中断、数量减少,同时可见许多细胞体积缩小,胞核固缩且染色加深。AD模型鼠海马CA1区AD模型组tau蛋白阳性细胞(62.13±4.1 2)个/HP,较健康对照组[(26.78±3.46)个/HP]与假手术组[(26.36±3.13)个/HP]明显增高(均P<0.01);MAP2阳性细胞吸光度值AD模型组为5.13±4.12,较健康对照组(28.78±3.46)与假手术组(29.36±3.13)明显减少,差异有统计学意义(均P<0.01)。结论在Aβ诱导的AD模型中tau蛋白表达增高,MAP2表达减低。更多还原

【Abstract】 Objective To establish the Alzheimer disease (AD) rat model with β-amyloid fragment 25-35 (Aβ25-35), and to observe the exepression of the tau protein and the microtubule-associated protein-2( MAP2) in the hippocampus. Methods The rat model of AD was established two weeks after injecting Aβ25-35 into the right hippocampus of rats. Then we examined the histological and immunohischemical changes of tau protein and MAP2 in CA1 subfield of the hippocampus. Results The pyramidal cell layers in CA1 of AD models become indiscriminate, sparse and discontinuous, the cells of which have shrinking soma, pycnotic nucleus and dark chromosomes. The tau-positive cells in the AD model group [(62. 13 ± 4. 12) Cells/HP] are obviously more than that in the normal control group [(26. 78 ± 3. 46) Cells/HP] or the sham operated group[(26. 36±3. 13) Cells/ HP] (P<0. 01) , while the MAP2-positive cells in the AD model group (5. 13 ± 4. 12) are obviously less than that in the normal control group (28.78 ± 3.46) or the sham operated group ( 29. 36 ± 3. 13) ( P < 0. 01). Conclusions The present study demonstrated the abnormal high expression of tau protein and the descent of MAP2 in the AD model induced by Aβ25-35 in rats, which are probably elements in the pathology of AD.更多还原