目的 考察舒脑欣滴丸对D-半乳糖造成阿尔茨海默病（AD）早期模型大鼠的神经保护作用及机制。方法 采用ip D-半乳糖（100 mg/kg）60 d造成大鼠AD早期模型，利用Morris水迷宫进行神经行为学检测，超氧化物歧化酶（SOD）和丙二醛（MDA）试剂盒测定氧化应激指标，免疫组织化学观察大脑皮质胶质纤维酸性蛋白（GFAP）和海马CA1区Caspase-3的表达，并利用HE染色观察脑海马区形态变化。结果 舒脑欣滴丸减少空间探索实验中模型大鼠的逃避潜伏期（P<0.05），增加穿越平台次数（P<0.05），显著性增加SOD活性（P<0.05），减少丙二醛MDA水平（P<0.05），并且能够降低大脑皮质GFAP的表达和海马CA1区Caspase-3的表达，同时能够改善模型大鼠的脑海马区形态。结论 舒脑欣滴丸对D-半乳糖造成的AD早期模型大鼠有一定的治疗作用，且其可能通过抗氧化应激、神经元凋亡和改善突触的连接及功能而起到神经保护作用。

Objective To investigate the neuroprotective effects of Shunaoxin Dropping Pill (SDP) on Alzheimer's disease (AD) rats induced by D-galactose their mechanisms. Methods Rats were ip given D-gal (100 mg/kg) for 60 d to induce the prominent changes of AD in the early stage. Morris water maze was used to investigate neurobehavioral changes, superoxide dismutase (SOD) and malondialdehyde (MDA) kits were used to determine the indicators of oxidative stress, immunohistochemistry was used to evaluate the expression of GFAP and Caspase-3, and HE staining was used to observe the morphological changes in hippocampal region. Results SDP treated group significantly decreased latency and increased the bouts of cross platform in Morris water maze experiment (P<0.05), improved the morphological changes in hippocampal region and significantly increased the content of SOD content (P<0.05), decreased the content of MDA (P<0.05), and alleviated the neuron death. Conclusion SDP has the certain therapeutic effect on prominent changes of AD in the early stage through its anti-oxidant stress effect. Our study provides the first piece of evidence supporting the potential use of SDP in the treatment of AD in clinic.