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目的:考察银杏达莫联合丁苯酞对Aβ_(1-42)致阿尔茨海默病(AD)模型大鼠记忆的影响及其可能机制。方法:将Aβ_(1-42)制备的AD大鼠随机分为模型组及银杏达莫2、4、6 m L/kg+丁苯酞40 mg/kg组,并设假手术组,每组20只,假手术组与模型组给予蒸馏水,给药30 d。结果:假手术组大鼠一般状态良好,模型组大鼠精神萎靡,活动迟缓,进食量少,体质量增长不明显,各给药组大鼠的状态介于模型组和假手术组间。与假手术组比较,模型组逃避潜伏期显著延长,脑组织SOD活性显著降低,OH·和胆碱酯酶活性显著升高(P<0.05),银杏达莫+丁苯酞可显著降低AD大鼠逃避潜伏期,提高脑组织SOD活性,降低脑组织OH·和胆碱酯酶活性(P<0.05)。与假手术组比较,模型组的海马组织tau表达明显升高,AKT和BNDF表达显著降低(P<0.05),与模型组比较,银杏达莫+丁苯酞组tau表达明显降低,AKT和BNDF表达显著升高(P<0.05)。结论:银杏达莫联合丁苯酞可显著改善AD的记忆能力,其机制可能与升高脑组织SOD活性,降低脑组织OH·和胆碱酯酶活性及调节脑内tau、AKT和BNDF的表达有关。
OBJECTIVE: To investigate the effect of ginkgoldolide and butylphthalide on the memory of Alzheimer’s disease (AD) model rats induced by Aβ 1-42 and its possible mechanism. Methods: AD rats were randomly divided into model group and ginkgoldol 2,4,6 m L / kg + butylphthalide 40 mg / kg group. The rats in sham operation group, 20 Only sham operation group and model group were given distilled water for 30 days. Results: The rats in sham-operation group were generally in good condition. The rats in model group were asymptomatic, sluggish, with low food intake and no significant increase in body weight. Rats in each administration group were in a state of between the model group and the sham operation group. Compared with the sham operation group, the escape latency of the model group was significantly prolonged, the activity of SOD in brain tissue and the activity of OH · and cholinesterase were significantly increased (P <0.05) Escaping from latent period, increasing SOD activity in brain tissue and decreasing OH · and cholinesterase activity in brain tissue (P <0.05). The expression of tau in hippocampus and the expression of AKT and BNDF in model group were significantly lower than those in sham operation group (P <0.05). Compared with model group, the expression of tau in ginkgo biloba and butylphthalide group was significantly decreased, while AKT and BNDF The expression was significantly increased (P <0.05). CONCLUSION: Ginkgo biloba combined with butylphthalide can significantly improve the memory ability of AD. The mechanism may be related to increasing SOD activity, decreasing OH · and cholinesterase activity and regulating brain tau, AKT and BNDF expression related.