D-半乳糖致老年性痴呆模型的评价和海马脑区甘丙肽表达研究

Evaluation on Alzheimer-like Disease Model Induced by D-galactose and Expression of Galanin in the Hippocampus

目的运用生化、组织、行为学方法评价D-半乳糖引发老年性痴呆(AD)小鼠模型,并测定其海马脑区甘丙肽的表达。方法选用C57小鼠,每天按体重150mg/kg经腹腔注射D-半乳糖,连续90d,制备AD痴呆动物模型。运用免疫荧光法检测甘丙肽表达,以生化方法检测乙酰胆碱酯酶(TChE)、胆碱乙酰转移酶(ChAT)、谷胱甘肽还原酶(GSH-PX)、超氧化物歧化酶(SOD)、丙二醛(MDA)、单胺氧化酶(MAO)等生化指标,通过透射电镜观察脑切片病理变化以及Y-型迷宫实验检测行为变化。结果与对照组相比,AD模型组小鼠脑内ChAT酶活性明显降低,脑细胞线粒体破裂,细胞核萎缩,学习记忆能力显著下降,海马脑区甘丙肽表达水平上升。结论D-半乳糖引发的小鼠AD模型在一定程度上模拟了AD的发病特点,可作为AD研究的一种模拟动物模型,模型组动物海马脑区甘丙肽呈高表达。

Objective To evaluate the Alzheimer-like disease （AD） mouse model induced by D-galactose with biochemical, histological, behavior methods, and to observe the expression of galanin in the hippocampus. Methods The C57 mice were injected with D-galactose （150mg/kg, i. p. 90 d） to make AD model. The Y-maze test, analysis of TChE. CHAT, GSH-PX. SOD. MDA. MAO and other enzymes, transmission electron microscopy （TEM） observation as well as the galanin expression with immunofluorescent assay were carried out to evaluate the mouse model for AD. Results Compared with the control group, the ChAT activity in the model group decreased, cell nuclear shrank and mitochondria spoiled, the ability of learning and memory decreased evidently, high expression of galanin in the hippocampus was detected with immunofluorescent assay. Conclusions The mouse model for AD induced by D-galactose simulated some characteristics of human AD to some extent and can he used as an approving animal model to study AD. Galanin expression in the hippocampus of the model group increased evidently.