Quantum dots protect against MPP＋-induced neurotoxicity in a cell model of Parkinson＇s disease through autophagy induction

作     者：Lu Wang Xiaoming Li Yuping Han Ting Wang Yun Zhao Aldalbahi Ali Nahed Nasser El-Sayed Jiye Shi Wenfeng Wang Chunhai Fan Nan Chen 

作者机构：Division of Physical Biology and Bioimaging CenterShanghai Synchrotron Radiation FacilityCAS Key Laboratory of Interfacial Physics and TechnologyShanghai Institute of Applied PhysicsChinese Academy of SciencesShanghai 201800China School of Life ScienceSichuan UniversityChengdu 610064China Chemistry DepartmentKing Saud UniversityRiyadh 11451Saudi Arabia School of Life Science and TechnologyShanghaiTech UniversityShanghai 201210China UCB PharmaSloughSL1 3WEUK 

出 版 物：《Science China Chemistry》 (中国科学（化学英文版）)

年 卷 期：2016年第59卷第11期

页      面：1486-1491页

核心收录：

学科分类：1002[医学-临床医学] 0703[理学-化学] 100204[医学-神经病学] 10[医学] 

基　　金：supported by the National Natural Science Foundation of China (U1332119, 31371015, 31470970) the Youth Innovation Promotion Association, CAS (2015211) Visiting Professor Program at King Saud University and the Shanghai Municipal Commission for Science and Technology (13NM1402300) 

主　　题：quantum dots autophagy Parkinson’s disease α-Synuclein Beclin1 

摘      要：Autophagy is a basic cellular process that decomposes damaged organelles and aberrant proteins. Dysregulation of autophagy is implicated in pathogenesis of neurodegenerative disorders, including Parkinson s disease(PD). Pharmacological compounds that stimulate autophagy can provide neuroprotection in models of PD. Nanoparticles have emerged as regulators of autophagy and have been tested in adjuvant therapy for diseases. In this present study, we explore the effects of quantum dots(QDs) that can induce autophagy in a cellular model of Parkinson s disease. Cd Te/Cd S/Zn S QDs protect differentiated rat pheochromocytoma PC12 cells from MPP+-induced cell damage, including reduced viability, apoptosis and accumulation of α-Synuclein, a characteristic protein of PD. The protective function of QDs is autophagy-dependent. In addition, we investigate the interaction between quantum dots and autophagic pathways and identify beclin1 as an essential factor for QDs-induced autophagy. Our results reveal new promise of QDs in the theranostic of neurodegenerative diseases.