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机构地区:[1]山东省胶南市人民医院保健科,山东胶南266400
出 处:《中国当代医药》2010年第6期9-10,共2页China Modern Medicine
摘 要:目的:探讨β淀粉样蛋白在小鼠D-半乳糖和氯化铝中毒模型中的变化及其机制。方法:使用D-半乳糖联合氯化铝制作阿尔茨海默病小鼠模型,于用药后0、45、60、75、90d取海马。取海马前用水迷宫实验分析小鼠的记忆和学习能力,对所取海马用改良的Bielschowsky氏银染来观察其病理改变。用Western杂交确定β淀粉样蛋白和BACE1蛋白的改变。结果:氯化铝和D-半乳糖处理的小鼠在水迷宫测试中逃避潜伏期明显延长;Bielschowsky氏银染发现海马细胞层次出现紊乱,但未发现典型的"老年斑"及"神经元纤维缠结";β淀粉样蛋白及BACE1的蛋白水平显著升高。结论:D-半乳糖及氯化铝可导致游离态的β淀粉样蛋白的生成增加,但并不能形成特征性的阿尔茨海默病样病理改变。Objective:To investigate the alteration of β-Amyloid and its mechanism in an animal model with D-galactose and AlCl3.Methods:Sixty kunming strain mice were separated into two equal groups randomly.One group was administered D-galactose and AlCl3 for 90 d,the control group with equivalent 0.9% NaCl.Morris water maze test was used to evaluate mice learning and memory.Hippocampus were stained using the bielschowsky staining procedure.BACE1 and A β protein level were measured by western blot.Results:Escape latency was prolonged significantly in D-galactose and AlCl3-treated mice in the morris water maze.Bielschowsky staining procedure found hippocampal cells was disorder.Western blot indicated that there was a tendency of increased Aβ and BACE1 expression.Conclusion:D-galactose and aluminum chloride can lead to the generation of free-state Aβ,but its increase alone can not form the Alzheimer's disease-like pathological changes.
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