烟酰胺单核苷酸腺苷酰转移酶1基因对原代培养小鼠神经元活力的影响  

Effect of nicotimamide monouncleotide adenylyl transferase 1 gene on vitality of cultured mouse neurons

作　　者：赵虹[1] 孙冬玲[2] 许美玲[1] 张惊宇[1] 赫丹丹[1] 

机构地区：[1]哈尔滨医科大学附属第四医院神经内科,哈尔滨150001 [2]鸡西市人民医院病理科,150001

出　　处：《中华神经医学杂志》2013年第10期973-975,共3页Chinese Journal of Neuromedicine

基　　金：黑龙江省教育厅科学技术研究项目资助（12521332）

摘　　要：目的评价烟酰胺单核苷酸腺苷酰转移酶I（NMNATl）基因对原代培养小鼠神经元活力的影响。方法取原代培养神经元，分成正常对照组、过表达NMNATl慢病毒感染组、RNA干扰慢病毒感染组，后两组分别感染小鼠NMNATl基因的过表达和RNA干扰慢病毒颗粒以上调和下调NMMT1基因的表达水平。应用MTT染色观察各组原代培养小鼠神经元活力的变化。结果与正常对照组原代培养小鼠神经元活力比较，过表达NMNAT1慢病毒感染组神经元的细胞活力显著增强，而RNA干扰慢病毒感染组神经元的细胞活力受到严重干扰，差异有统计学意义（P=0．025．P=0．027）。结论NMNAT1基因在神经元发育过程中起重要作用，其缺失可能导致中枢神经系统的神经退化。Objective To evaluate the effect of nicotinamide mononucleotide adenylyl transferase 1 （NMNA T1） gene on vitality of cultured mouse neurons. Methods Culture of primary mouse neurons in vitro was set up and the neurons were divided into normal control group, NMNA T1 over-expression group and knocking down of NMNA T1 by RNA interference group; the expression level of NMNA T1 in the three groups were detected, and then the vitality of neurons was tested by MTT assay. Results As compared with that in the normal control group, the NMNA T1 over-expression group had increased neuronal vitality, while knocking down of NMNA T1 by RNA interference group had decreased neuronal vitality in vitro, with significant differences （P=-0.025, P=0.027）. Conclusion There is a novel role for NMNA T1 in the morphogenesis of developing neurons, which indicates that the loss of function of NMNA T1 may contribute to different neurodegenerative disorders in central nervous system.

关 键 词：烟酰胺单核苷酸腺苷酰转移酶1 原代培养神经元 神经元活力 神经系统退 行性疾病 

分 类 号：R329[医药卫生—人体解剖和组织胚胎学]