中文摘要：

目的 使用雷帕霉素保护神经退行性疾病损伤模型中神经元的线粒体从而降低神经元的损伤.方法 建立帕金森氏症（PD）细胞和动物的损伤模型,在损伤模型中加入雷帕霉素,经染色后于激光共聚焦显微镜下观察雷帕霉素诱导细胞自噬作用、对线粒体膜极性变化的作用、对细胞内活性氧（ROS）的清除作用以及NF-κB的入核情况.结果 雷帕霉素能诱导细胞自噬在MPP＋诱导的细胞损伤中,并能维持线粒体的正常形态、降低线粒体膜电位的变化、降低细胞ROS水平并减少NF-κB的入核.此外,雷帕霉素在MPTP诱发的斑马鱼和小鼠PD模型中对神经元有显著保护作用.结论 雷帕霉素能通过诱导细胞自噬作用于线粒体从而保护神经元免于神经退行性疾病的损伤,加强对线粒体的保护是一种治疗神经退行性疾病的新思路.

英文摘要：

Objective Using rapamycin protecting neurons＇ mitochondrial within injury model of neurodegenerative disease thus to reduce neuronal damage.Methods Parkinson＇s disease （PD） injury model of cells and animals were established,then rapamycin was added,and induced autophagy,the polarity changes of mitochondrial membrane potential,intracellular reactive oxygen species （ROS） scavenging and the contents of NF-κB inside the nucleus after dyeing were observed by confocal laser scanning microscopy.Results Rapamycin can induce autophagy and maintain morphology of mitochondria in cells damaged by MPP＋.Mitochondrial membrane potential,level of ROS and contents of NF-κB inside the nuclear can be detected obviously reduced in these cells with rapamycin＇ s function.Furthermore,rapamycin also protects neurons well within PD models of zebrafish and mouse which are damaged by MPTP.Conclusions Rapamycin induces autophagy and protects mitochondria from damage within neurodegenerative disease,and strengthening this kind of protection of mitochondria is a novel way to deal with neurodegenerative diseases.