重组人Semaphorin3A诱导体外培养的大鼠大脑皮层神经元轴突损伤的实验研究  

Recombinant human Semaphorin 3A induces axon injuries in cultured rat cerebral cortical neurons

作　　者：陶玉倩[1] 田青[1] 叶文华 杨颖[1] 张赛[1] 

机构地区：[1]中山大学附属第一医院神经科,广东广州510080 [2]佛山市南海区人民医院,广东佛山528200

出　　处：《中风与神经疾病杂志》2010年第12期1068-1071,共4页Journal of Apoplexy and Nervous Diseases

基　　金：广东省自然科学基金项目(No.9151066302000004);广东省自然科学基金项目(No.06021357)

摘　　要：目的探讨外源性Semaphorin3A（Sema3A）对于体外培养神经元轴突生长及神经元生长活性的影响。方法体外培养新生SD大鼠皮质神经元,随机分为正常对照组和Sema3A不同浓度处理组,倒置相差显微镜及微管相关蛋白-2（MAP-2）荧光染色分别观察生长锥及轴突形态学变化;噻唑蓝（MTT）法检测神经元存活率。结果 Sema3A（0.5mg/ml）处理可诱发神经元生长锥崩解;与正常对照组相比,Sema3A（5mg/ml）处理组轴突平均长度缩短（P〈0.001）;经不同浓度Sema3A处理后,神经元存活率呈剂量依赖性下降,其中浓度范围为0.5-5.0mg/ml的处理组与正常组比较均有统计学意义（P〈0.001）。结论 Sema3A在体外可发挥明显的促生长锥崩解及抑制轴突生长的作用,并且具有一定的神经元毒性。Objective To investigate the effect of exogenous Semaphorin 3A（Sema3A）on axon outgrowth and neuronal growth activity in vitro.Methods Cultured cortical neurons of newborn SD rats were randomly divided into control group and treatment group with various concentrations of Sema3A.Morphological changes of growth cones and axons were observed with inverted phase contrast microscope and microtubule associated protein-2（MAP-2） staining respectively.Neuronal survival rate was assayed with MTT method.Results Treatment of Sema3A（0.5mg/ml） could induce neuronal growth cone to collapse.Compared with the normal control group,the average axon length of treatment group with Sema3A（5mg/ml） was shortened（P〈0.001）.Treated with various concentrations of Sema3A,the neuron survival rate reduced in a dose-dependent manner.The difference between control group and each treatment group with a range of 0.5-5.0mg/ml concentration was statistically significant（P〈0.001）.Conclusion Sema3A can play a significant role in vitro in promoting growth cone collapse and inhibition of axon outgrowth,with neuron toxicity additionally.

关 键 词：Semaphorin3A 大脑皮层神经元 生长锥 轴突/损伤 

分 类 号：R363[医药卫生—病理学]