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Previous studies have demonstrated that ubiquitin-proteasome system function is significantly decreased in the substantia nigra of Parkinson’s disease patients.In the present study,proteasome inhibitor Z-Ile-Glu(OtBu)-Ala-Leucinal(PSI)was used to inhibit the function of the ubiquitin-proteasome system in PC12 cells to simulate Parkinson’s disease.Oxidatively modified proteins were identified to determine pathogenesis of Parkinson’s disease.Results demonstrated that 24 hours of 10μmol/L PSI-treatment in PC12 cells simulated pathological characteristics of Parkinson’s disease:neuronal degeneration and eosinophilic inclusion formation in neurons.In PSI-treated PC12 cells,three oxidative proteins and a molecular chaperone family member were detected:chaperonin containing t-complex polypeptide 1 subunit 3,glucose-regulated protein 58,and heat shock protein 70.This is the first study to demonstrate oxidative modification of a molecule family in a cell model of Parkinson’s disease induced with PSI.
Previous studies have demonstrated that ubiquitin-proteasome system function is significantly less in the substantia nigra of Parkinson’s disease patients. In the present study, proteasome inhibitor Z-Ile-Glu (OtBu) -Ala-Leucinal (PSI) was used to inhibit the function of the ubiquitin-proteasome system in PC12 cells to simulate Parkinson’s disease. Oxidatively modified proteins were identified to determine pathogenesis of Parkinson’s disease. Results for that 24 hours of 10 μmol / L PSI-treatment in PC12 cells simulated pathological characteristics of Parkinson’s disease: neuronal degeneration and eosinophilic inclusion formation in neurons. In PSI-treated PC12 cells, three oxidative proteins and a molecular chaperone family member were detected: chaperonin containing t-complex polypeptide 1 subunit 3, glucose-regulated protein 58, and heat shock protein 70. the first study to demonstrate oxidative modification of a molecule family in a cell model of Parkinson’s disease induced wi th PSI.