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目的:观察灵芝多糖(GLP)对阿尔茨海默病(AD)模型大鼠海马内突触及突触素表达的影响。方法:清洁级雄性SD大鼠,双侧海马内一次性注射β-淀粉样多肽25～35片段(Aβ25～35)制作大鼠AD模型;ip不同浓度的灵芝多糖溶液进行治疗,连续7 d,每天1次;Morris水迷宫检测动物学习记忆能力,采用免疫组织化学染色法、透射电镜技术结合图象分析方法比较各组大鼠海马CA1,CA3区突触素表达、突触的数密度和面密度变化。结果:与模型组相比,灵芝多糖75,50 mg.kg-1能显著降低大鼠水迷宫实验的平均潜伏期,升高跨越平台次数;亦能显著升高大鼠海马突触素的表达(P<0.01)及突触的数密度(Nv)和面密度(Sv)(P均<0.01)。结论:灵芝多糖能显著升高老年性痴呆(阿尔茨海默病)大鼠海马内降低的突触素/突触,此可能是增强大鼠学习记忆产生抗痴呆作用的机制之一。
Objective: To observe the effects of Ganoderma lucidum polysaccharides (GLP) on the synaptic and synaptophysin expression in the hippocampus of Alzheimer’s disease (AD) model rats. Methods: The AD models of rats were made by injecting 25-35 β-amyloid peptides (Aβ25-35) in clean male SD rats and bilateral hippocampus. The rats were treated with different concentrations of Ganoderma lucidum polysaccharides for 7 days, Once a day. Morris water maze was used to detect the learning and memory abilities of animals. Immunohistochemical staining, transmission electron microscopy and image analysis were used to compare the synaptophysin expression in hippocampal CA1 and CA3 areas. Density changes. Results: Compared with the model group, Ganoderma lucidum polysaccharides 75,50 mg.kg-1 can significantly reduce the average latency of water maze test and increase the number of platforms across the platform; also significantly increased the expression of synaptophysin (P <0.01) and synaptic number density (Nv) and areal density (Sv) (P <0.01). CONCLUSION: Ganoderma lucidum polysaccharides can significantly decrease the concentration of synaptophysin / synapse in the hippocampus of Alzheimer’s disease rats, which may be one of the mechanisms of enhancing the anti-dementia effect of learning and memory in rats.