CAJ | 학술논문

目的建立帕金森病(PD)多巴胺能神经元轴突变性新的体外实验细胞模型.方法检测不同浓度1-甲基-4-苯基吡啶离子(MPP+)致原代培养的小鼠中脑腹侧多巴胺神经元损伤的能力.采用免疫组织化学的方法检测轴突的形态学变化、存活神经元的数目、轴突的长度和数目,以及凋亡多巴胺神经元的数目.噻唑蓝(MTT)比色检测细胞活力在MPP+处理2～24h的不同时间点进行.结果 10.0μmol/L的MPP+作用24 h导致多巴胺神经元显著的轴突变性.神经元的数目、轴突的长度和数目均分别减少50.39％、59.80％、35.70％.结论 10.0 μmol/L的MPP+作用24 h造成的体外实验模型可以有效地反映帕金森病的轴突变性.
목적 건립파금삼병(PD)다파알능신경원축돌변성신적체외실험세포모형.방법 검측불동농도1-갑기-4-분기필정리자(MPP+)치원대배양적소서중뇌복측다파알신경원손상적능력.채용면역조직화학적방법검측축돌적형태학변화、존활신경원적수목、축돌적장도화수목,이급조망다파알신경원적수목.새서람(MTT)비색검측세포활력재MPP+처리2～24h적불동시간점진행.결과 10.0μmol/L적MPP+작용24 h도치다파알신경원현저적축돌변성.신경원적수목、축돌적장도화수목균분별감소50.39％、59.80％、35.70％.결론 10.0 μmol/L적MPP+작용24 h조성적체외실험모형가이유효지반영파금삼병적축돌변성.
Objective To establish an in vitro model of the axonal degeneration of dopaminergic neurons in parkinson' s disease (PD).Methods A variety of concentrations of 1-methyl-4-phenylpyridinium (MPP +) were tested for their ability to induce injury of primary cultured dopaminergic neurons from the mouse ventral mesencephalon.Morphological changes to axons,the number of remaining neurons,the length and number of axons,and the number of apoptotic dopaminergic neurons were observed by immunohistochemistry,methyl thiazol tetrazolium (MTT) assays was performed to determine the cell viability at different time points from 2 h to 24 h after addition of MPP +.Results Exposure of dopaminergic neurons to 10.0 μmol/L MPP + for 24 h caused significant axonal degeneration.The number of neurons,axon length and the number of axons were respectively decreased by 50.39％,59.80％,and 35.70％.Conclusion An in vitro model in which cells are treated with 10.0 μmol/L MPP+ for 24 h can be used as an effective model of the axonal degeneration of dopaminergic neurons in PD.