SMND-309对神经元轴突可塑性作用的研究  

The effect of SMND-309 on axonal plasticity

作　　者：王友磊[1] 张瑾锦[2] 

机构地区：[1]滨州医学院特教学院,烟台264003 [2]滨州医学院医学研究中心

出　　处：《滨州医学院学报》2012年第5期328-331,共4页Journal of Binzhou Medical University

基　　金：滨州医学院科技计划项目(BY2008KJ05);山东省教育厅科技计划项目(J11FL87)

摘　　要：目的研究SMND-309对轴突可塑性的影响,并探讨其可能的作用机制。方法体外培养SH-SY5Y细胞,全反式维甲酸(ATRA)诱导细胞分化,轻度氧糖剥夺再灌注(OGD/R)损伤轴突,测量SMND-309干预后轴突长度的变化;Western blot-ting技术检测胞内BDNF、t-Akt、p-Akt含量的变化。结果轻度OGD/R之后,轴突长度缩短明显(P<0.01),胞内t-Akt含量无显著变化(P>0.05),p-Akt稍有下调(P>0.05)、BDNF水平显著下调(P<0.05);0.5μmol/L SMND-309干预后,轴突增长,p-Akt、BDNF含量显著上调(P<0.01),LY294002预处理后,SMND-309的作用受到显著抑制(P<0.01)。结论 SMND-309能显著的促进OGD/R之后轴突的可塑性,这种作用可能与通过PI3K/Akt信号通路提高胞内BDNF的水平有关。Objective To study the effect of SMND-309 on axonal plasticity and discuss the possible mechanism.Methods SH-SY5Y cells were differentiated into neuron-like phenotype with long axon by all-trans retinoic acid,and then axons were insulted in vitro with maintaining the cells under mild OGD/R condition.The length of axons were measured after administration with SMND-309.The levels of intracellular BDNF,t-Akt,p-Akt were detected by Western blotting.Results The length of axons was significantly shorten（P0.01） in mild OGD/R.There was no significant change in the expression of intracellular t-Akt（P0.05）,and the p-Akt were generous down-regulated versus the control（P0.05）,but the level of BDNF was markedly down-regulated（P0.05）.Treated with 0.5 μmol/L SMND-309,the length of axons were longer than that of cells in OGD/R（P0.01）,The dose of 0.5 μmol/L SMND-309 could up-regulate significantly the level of p-Akt and BDNF（P0.01）,while the positive role of SMND-309 was inhibited by incubcation with LY294002（P0.01）.Conclusion SMND-309 was able to increase intracellular BDNF and promote axonal plasticity after OGD/R which was possibly accomplished through PI3K/Akt signal pathway.

关 键 词：SMND-309 SH-SY5Y细胞 轴突重构 信号通路 

分 类 号：R338[医药卫生—人体生理学]