【摘要】 目的:采用铝负荷致小鼠脑损伤模型,探讨铝致神经元退行性变与脑单胺氧化酶B代谢失衡的关系。方法:每鼠侧脑室内分别注射浓度为0.125%、0.25%、0.5%的AlCl3 3μl,连续给药5天,建立不同量铝过负荷致脑损伤小鼠模型。于给药后第10天、第20天和第30天测定小鼠学习记忆功能、海马病理形态学改变、单胺氧化酶B(Monoamine oxidase B,MAO-B)活性。结果:铝过负荷致小鼠脑内MAO-B活力显著升高和CA1区出现明显神经元丢失及核固缩;上述指标均呈剂量依赖性和时间依赖性改变。结论:铝过负荷致神经元退变可能与其干扰脑单胺氧化酶B代谢有关。更多还原

【Abstract】 Objective:To adopt the brain lesion model of mouse induced by overload aluminum to study the relationship between monoamine oxidase B disorder and neurodegeneration induced by overload aluminum(Al).Method:Aluminum overload models were established by injection of 3μl AlCl3 into lateral ventricle of miceeach day for 5d.The AlCl3 solutions injected in different modelswere with different concentrations and they were 0.125%,0.25%,0.5%.On d10,d20,and d30 after the final administration of AlCl3 solution,the learning and memory function of mice,pathomorphology of hippocampi,and MAO-B activity were determined.Results:Aluminum overload elevated MAO-B activity,caused karyopyknosis and loss of neurons in CA1 area of hippocampi,in dose-and time-dependent manners.Conclusion:The results indicate that neurodegeneration induced by Al toxicity may be related to the monoamine oxidase B homeostasis interfered by Al overload.更多还原