目的:探求地黄饮子对AD模型大鼠脑内Aβ生成的干预机制。方法:清洁级健康雄性Wistar大鼠100只,随机取10只为空白组,其余90只随机平均分为6组:假手术组,模型组,西药组,中药高、中、低剂量组,每组15只。各组腹腔注射D-gal 4周,西药组给予盐酸多奈哌齐,中药高、中、低剂量组给予高、中、低剂量地黄饮子,模型组、假手术组给予等量0.9%氯化钠溶液灌胃。4周后,药物干预组大鼠在海马坐标区注射Aβ_(1-40),假手术组大鼠在上述部位注射0.9%氯化钠溶液。1周后HE染色和免疫组化法观察脑组织中β-淀粉样蛋白相关因子水平。结果:各组模型大鼠β-APP、BACE及Aβ免疫组化染色示,模型组表达显著升高(P<0.01);与模型组相比中药各剂量组均可显著下调β-APP、BACE及Aβ的表达(P<0.01);各药物组间比较以中药高剂量组为优。结论:地黄饮子能够抑制β-APP经由淀粉样肽源性途径的裂解过程,使Aβ在脑组织中的表达水平降低。 Objective: To explore the intervention mechanism of Rehmanniae Decoction on Aβ production in brain of AD model rats. Methods: One hundred healthy male Wistar rats were randomly divided into blank group (n = 10) and blank control group (n = 10). The remaining 90 patients were randomly divided into 6 groups: sham operation group, model group, western medicine group, Group of 15. The rats in each group were intraperitoneally injected with D-gal for 4 weeks. The western medicine group was treated with donepezil hydrochloride. The rats in the high, middle and low dose groups were given high, medium and low doses of Rehmanniae. The rats in the model group and sham operation group were given 0.9% sodium chloride solution Gavage. Four weeks later, the rats in the drug-treated group were injected with Aβ 1-40 in the hippocampus and the rats in the sham-operated group were injected 0.9% sodium chloride solution at the above site. One week later, HE staining and immunohistochemistry were used to observe the levels of β-amyloid-related factors in brain tissue. Results: Compared with the model group, the expression of β-APP, BACE and Aβ in the model group was significantly increased (P <0.01) And the expression of Aβ (P <0.01). The high dose group of Chinese medicine group was the best among all the drug groups. Conclusion: Rehmanniae Decoction can inhibit the release of β-APP through the amyloid peptide-derived pathway and decrease the expression of Aβ in brain tissue.