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目的探讨过氧化氢(H2O2)对多巴胺能神经元的选择性损伤作用。方法用神经生长因子将PC12细胞诱导分化成多巴胺能神经元模型,以N2a细胞作为对照,2组细胞共同经H2O2处理后,在激光扫描共聚焦显微镜下观察细胞内α-synuclein异常修饰和聚集以及细胞形态改变;PC12细胞经利血平耗竭多巴胺后用H2O2处理,并观察α-synuclein异常修饰和聚集及细胞形态变化。结果H2O2处理的PC12细胞胞浆内逐渐出现泛素化的α-synuclein聚集,细胞轴突回缩消失,胞体变圆、变小,胞核变大,N2a细胞及利血平耗竭多巴胺的PC12细胞经H2O2处理后细胞胞浆内无α-synuclein聚集。结论H2O2能选择性引起多巴胺能神经元胞浆内泛素化α-synuclein蛋白的异常聚集,并导致细胞退行性变,该现象可能与神经元内源性多巴胺有关。
Objective To investigate the selective injury of dopaminergic neurons by hydrogen peroxide (H2O2). Methods PC12 cells were induced to differentiate into dopaminergic neurons by using nerve growth factor (NGF). N2a cells were used as control. Two groups of cells were treated with H2O2. Abnormal modification and aggregation of α-synuclein in cells were observed under laser scanning confocal microscopy. Cell morphology changes; PC12 cells after reserpine depletion of reserpine H2O2 treatment, and abnormal changes and aggregation of α-synuclein and cell morphology was observed. Results In the cytoplasm of PC12 cells treated with H2O2, ubiquitinated α-synuclein gradually accumulated in the cytoplasm, and the axons retracted and disappeared. The cell bodies became round and became smaller, and the nuclei became larger. The apoptosis of N2a cells and reserpine-depleted PC12 cells After H2O2 treatment, there was no accumulation of α-synuclein in the cytoplasm. Conclusion H2O2 can selectively induce the abnormal aggregation of ubiquitinated α-synuclein in the cytoplasm of dopaminergic neurons and lead to the degeneration of cells. This phenomenon may be related to the endogenous dopamine in neurons.