目的 考察海马补肾丸对小鼠学习记忆障碍的改善作用，并探讨其作用机制。方法 小鼠随机分为对照组、模型组、吡拉西坦组、龟龄集组和海马补肾丸组。采用腹腔注射东莨菪碱制备小鼠记忆获得性障碍模型，计算学习正确率，测定蛋白含量和乙酰胆碱酯酶活力。采用腹腔注射亚硝酸钠制备小鼠记忆巩固性障碍模型，计算训练、测定学习正确率，测定蛋白含量、去甲肾上腺素（NE）、多巴胺（DA）、5-羟色胺（5-HT）以及丙二醛（MDA）、超氧化物歧化酶（SOD）含量。结果 海马补肾丸2.20 g/kg组能显著增加小鼠学习记忆的正确率（P<0.05），显著降低乙酰胆碱酯酶活力（P<0.01）。测定时，与模型组比较，海马补肾丸1.10、2.20 g/kg组能显著增加小鼠学习记忆正确率（P<0.05），能不同程度增加小鼠大脑SOD含量，降低MDA含量（P<0.05、0.01）。结论 海马补肾丸能明显改善小鼠的记忆获得、记忆巩固障碍，推测其作用机制主要是通过降低乙酰胆碱酯酶活性，增加脑内乙酰胆碱的含量，改善记忆获得能力；通过抗脑组织的氧化损伤，增加大脑SOD含量，降低MDA含量，改善记忆巩固能力。

Objective To investigate the improvement on Haima Bushen Pills on learning and memory impairment in mice, and study its mechanism. Methods Mice were randomly divided into control group, model group, piracetam group, Guilingji group, and Haima Bushen Pills group. The model of memory acquired impairment in mice was established by intraperitoneal injection of scopolamine. The correct rate of learning was calculated, and the protein content and acetylcholinesterase activity were determined. The memory consolidation impairment model of mice was induced by intraperitoneal injection of sodium nitrite. The learning accuracy of training and determination was calculated, and the protein content, NE, DA, 5-HT, MDA and SOD content were determined. Results Haima Bushen Pills (2.20 g/kg) group could significantly increase the correct rate of learning and memory in mice (P < 0.05), and significantly reduce the activity of acetylcholinesterase (P < 0.01). Compared with the model group, Haima Bushen Pills (1.10, 2.20 g/kg) group could significantly increase the correct rate of learning and memory in mice (P < 0.05), and increase SOD content and decrease MDA content in mice brain (P < 0.05, 0.01). Conclusion Haima Bushen Pills can significantly improve memory acquisition and memory consolidation disorders in mice. Its mechanism is maybe mainly through reducing the activity of acetylcholinesterase, increasing the content of acetylcholine in the brain and improving the ability of memory acquisition. And improve the memory consolidation by resisting oxidative damage of brain tissue, increasing SOD and reducing MDA content in brain.