铝负荷致小鼠神经元退行性病变的实验研究

Experimental Study on Neurodegeneration Induced by Aluminum Overload in Mice

目的研究铝负荷致小鼠神经元退行性病变的量-效和时-效关系及相关指标的变化。方法小鼠侧脑室内注射3μl AlCl3建立铝负荷致神经元退行性变模型。以跳台和水迷宫法评价学习记忆成绩;以常规HE染色观察海马病理变化;以等离子体原子发射光谱法测定脑内总铝与总锰水平;以海马胆碱酯酶(ChE)和单胺氧化酶B(MAOB)活力作为生化评价指标。结果与对照组相比,铝负荷组小鼠下台潜伏期和寻台时间分别呈剂量和时间依赖性明显缩短或延长;海马ChE和MAOB活力明显升高,脑总锰水平也明显升高;病理切片显示,铝负荷组小鼠海马CA1和CA3区出现神经元核固缩和神经元减少,且表现出与铝负荷剂量和时间依赖性相关的加重趋势。结论铝过负荷致小鼠出现明显神经元退行性病变和学习记忆能力障碍;这些变化至少可能与脑ChE和MAOB活力增强及脑内锰水平升高有关。

Objective To explore the dose-effect and time-effect relationship of neurodegeneration induced by aluminum overload and the changes of relative parameters in mice. Methods An animal model was established by icy trace AlCl3 into mouse lateral ventricle. The passive avoidance learning and spatial learning abilities of mice, eholinesterase （ChE） and monoaminoxidase B （MAOB） activities and pathomorphological changes in hippocampi, as well as the magnesium （Mn） levels in brain were evaluated. Results Overload aluminum significantly shortened step-down latency and prolonged platform-seeking time, increased the activities of ChE and MAOB in hippocampi, caused karyopyknosis and loss of hippocampal neurons, and raised Mn level of brain. The learning and memory functions of mice in the experimental groups were markedly damaged. Conclusions The aluminum overload could obviously induce neurodegeneration and learning and memory disorders of mice. All changes above are at least related to increasing activities of ChE and MAOB, as well as promoting Mn level in brain.