【摘要】 目的:探讨泛素-蛋白酶体系统(UPS)功能障碍诱发帕金森病(PD)细胞模型的作用机制,为深入研究PD的发病机制提供理论依据。方法:建立PSI诱导的PC12细胞模型,实验组、对照组分别加入PSI和DMSO(终浓度为10μmol.L-1)孵育36 h后提取蛋白,应用荧光差异凝胶电泳(DIGE)系统获得差异蛋白点,运用基质辅助激光解吸/电离飞行时间质谱仪(MALDI-TOF Pro MS)鉴定出差异蛋白。结果:实验组与对照组比较,在36 h可见细胞内嗜酸性类Lewy小体形成及细胞凋亡(细胞核呈固缩状或碎裂状),凋亡百分率为25.53%。实验组内质网蛋白ERp29与对照组比较表达量显著降低,差异有显著性(P<0.01)。结论:内质网应激(ERS)在UPS功能障碍引起PD的病理变化过程中起重要作用。更多还原

【Abstract】 Objective To investigate the pathogenetic mechanism of ubiquitin-proteasome dysfunction in a model of Parkinson’s disease(PD),which can provide the theoretical basis for PD.Methods After establishment of PD model induced by PSI in PC12 cells,proteins of untreated(DMSO) and PSI-treated PC12 cells were extracted 36 h after incubation,and then the maps of the extracted proteins were established by DIGE system.The altered protein spots were identified with MALDI-TOF Pro MS and database searching.Results Thirty-six treatment of PC12 cells with PSI induced the appearance of cytoplasmic Lewy body-like eosinophilic inclusions and apoptosis.The percentage of apoptotic cells was 25.53%.ERp29 were identified by MALDITOF Pro MS.The expression of ERp29 decreased in treatment group,compared with normal group(P<0.01).Conclusion Endoplasmic reticulum stress(ERS) may play an important role in the pathogenesis of ubiquitin-proteasome system dysfunction induced PD.更多还原