目的 探讨补肾化痰益智法（BSHTYZ）对阿尔茨海默病（Alzheimer’s Disease， AD）样模型大鼠认知障碍的改善及分子机制。方法 通过对Sprague Dawley（SD）雄性大鼠侧脑室内注射Aβ_1-42构建AD大鼠模型，分别用低（12.5g/kg·d，BSHTYZ-L）、中（25 g/kg·d，BSHTYZ-M）、高（50 g/kg·d，BSHTYZ-H）剂量的补肾化痰益智方水煎液灌胃，分2次灌服，同时设置对照组、模型组和阳性治疗组，4周后利用Morris水迷宫和改良Highman刚果红染色分别观察AD模型大鼠空间学习记忆能力和Aβ在大脑皮层和海马的分布情况，同时利用Western blot检测补肾化痰益智法对AD模型大鼠海马区APP、pAPP668及其α、β、γ分泌酶和降解酶IDE等蛋白表达的影响。结果 通过大鼠侧脑室注射Aβ_1-42，可诱导出大鼠AD样空间学习记忆障碍、大脑皮层和海马的海马Aβ沉积增加及pAPP668表达增加，同时可见α分泌酶和IDE降解酶减少、β分泌酶的水平上升，中高剂量的补肾化痰益智方干预后均能显著逆转上述现象，同时高剂量补肾化痰益智方还能降低γ分泌酶的水平。结论 补肾化痰益智法能有效改善Aβ_1-42引起的AD样模型大鼠的学习记忆能力减退，其保护机制可能通过减少Aβ的生成、增加Aβ的降解从而缓解Aβ在脑内的聚集来调控APP的代谢有关。

Objective To study the effect and mechanism of Bushen Huatan Yizhi Method (BSHTYZ) on cognitive impairment of the Alzheimer"s Disease (AD) model rats.Methods Alzheimer"s Disease model was established by injection of β-amyloid protein 1-42 (Aβ_1-42) in the left lateral ventricles of Sprague Dawley (SD) rats. The rats were treated with low (12.5 g/kg·d, BSHTYZ-L), medium (25 g/kg·d,BSHTYZ-M) and high (50 g/kg·d, BSHTYZ-H) dose of prescription of Bushen Huatan Yizhi, then the Morris water maze, modified highman Congo red staining and Western blot methods were used to detect the ability of learning and memory, the deposition of Aβ and the levels of APP, pAPP668, α secretase (ADMA10), β secretase (BACE1), γ secretase (PS1) and insulin degrading enzyme (IDE) in the hippocampus.Results Middle and high doses of prescription of BSHTYZ could effectively reverse the decreased ability of learning and memory, increase the deposition of Aβ with the level of pAPP668 and BACE1, decrease the level of ADMA10 and IDE of the hippocampus induced by Aβ_1-42.Conclusion Prescription of BSHTYZ plays a role of neuroprotection of the cognitive impairment of AD like model of rats induced by Aβ_1-42, and the protective mechanism may be related to the regulation of APP metabolism by reducing the production and increasing the degradation of Aβ to alleviate the aggregation of Aβ in the brain.