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目的探讨蛋白酶体抑制剂(Proteasome inhibitor,PSI)诱导的PC12细胞帕金森病(Parkinson disease,PD)模型中血红素加氧酶-1(Hemeoxygenase-1,HO-1)的差异表达,为深入研究PD的发病机制提供理论依据。方法取培养的PC12细胞,加入终浓度为10μmol/L的PSI,建立PSI诱导的PC12细胞模型,以加入终浓度为10μmol/L的二甲基亚砜(DMSO)为对照组。经HE、AO&EB及α-SYN染色进行鉴定;PSI作用48h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-TOFProMS)鉴定差异蛋白。结果模型组与对照组比较,PSI作用48h可见细胞内嗜酸性类Lewy小体形成及细胞凋亡,凋亡率达(24.74±4.55)%。模型组与对照组比较,HO-1表达量显著增加。结论在泛素-蛋白酶体系统(Ubiquitin-proteasome system,UPS)功能障碍诱发PD过程中,氧化应激反应发挥着一定的作用。
Objective To investigate the differential expression of hemeoxygenase-1 (HO-1) in the Parkinson disease (PD) -induced PC12 cells induced by proteasome inhibitor (PSI) PD pathogenesis provides a theoretical basis. Methods The cultured PC12 cells were treated with PSI at a final concentration of 10μmol / L to establish a model of PC12 cells induced by PSI. DMSO was added as the control at a concentration of 10μmol / L. Identified by HE, AO & EB and α-SYN staining. After PSI for 48h, the proteins were extracted and differentially expressed proteins were obtained by using DIGE system. MALDI-TOF-MS Identify differential proteins. Results Compared with the control group, the formation of eosinophilic Lewy bodies and the apoptosis in the model group were observed after treated with PSI for 48 hours. The apoptotic rate reached 24.74 ± 4.55%. Compared with the control group, the expression of HO-1 in the model group increased significantly. Conclusions Oxidative stress plays a role in PD induced by dysfunction of ubiquitin-proteasome system (UPS).