去痴灵对AD模型小鼠学习记忆及脑内突触体素表达的影响

目的 观察去痴灵对阿尔茨海默病(AD)小鼠学习记忆以及脑内突触体素(synaptophysin,SYN)表达的影响.方法 选用昆明种小鼠,右侧脑室注射β-淀粉样蛋白25-35(Aβ25-35)制备AD动物模型.造模1 w后,治疗组分别灌胃低、中、高剂量(3.05、6.10、12.20 g·kg~(-1)·d~(-1))去痴灵,以石杉碱甲为阳性对照药,连续28 d.给药结束后,对各组小鼠进行Morris水迷宫测试、脑组织SYN含量测定以及海马CA1区病理结构观察.结果 与模型组比较,去痴灵各剂量组均明显缩短水迷宫逃避潜伏期(P<0.05),中、高剂量组跨越平台次数显著增加(P<0.05);各治疗组AchE阳性纤维密度明显增加(P<0.05),脑内SYN含量明显升高(P<0.05),突触结构改善明显;各治疗组上述指标组间比较差异不显著(P>0.05).结论 去痴灵可明显改善Aβ所致的小鼠记忆障碍及突触丧失,其脑内突触再生,突触体素含量增加可能是去痴灵改善AD记忆的重要途径之一.

Effects of Quchiling on learning and memory and synaptophysin expression of brain in Alzheimer's disease (AD) model mice

Objective To investigate the effects of Quchiling on the learning and memory and synaptophysin(SYN) expression of brain in Alzheimer's disease (AD) model mice.Methods AD mice model was established by β-amyloid peptide 25-35 injection into right lateral ventricle.One week later,the therapeutic groups were given Quchiling through gastric gavage for 28 days.Huperzine A was used as a positive control drug.Subsequently,the test of Morris water-maze,the expression of SYN,the dense of AchE!positive fibrils and the observation of ultrastructure of synapses in brain were applied to evaluate the effects of Quchiling on the AD model mice.Results Compared with AD model group,the mice administered by different doses of Quchiling had shorter escape latency and more platform-crossing times except the group treated with low dose Quchiling (P<0.05).Furthermore,Quchiling increased the dense of AchE positive fibrils and upregulated the expression of SYN (P<0.05).There was no remarkably difference between all the therapeutic groups (P>0.05).Conclusions Quchiling increases the content of the cerebric SYN,and restores the impaired synapse structure,which maybe contributed to the improvement of learning and memory in the mice with AD.