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 

机构地区：[1]Division of Physical Biology and Bioimaging Center,Shanghai Synchrotron Radiation Facility,CAS Key Laboratory of Interfacial Physics and Technology,Shanghai Institute of Applied Physics,Chinese Academy of Sciences,Shanghai 201800,China [2]School of Life Science,Sichuan University,Chengdu 610064,China [3]Chemistry Department,King Saud University,Riyadh 11451,Saudi Arabia [4]School of Life Science and Technology,ShanghaiTech University,Shanghai 201210,China [5]UCB Pharma,Slough,SL1 3WE,UK

出　　处：《Science China Chemistry》2016年第11期1486-1491,共6页中国科学（化学英文版）

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)

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.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.

关 键 词：quantum dots AUTOPHAGY Parkinson’s disease Α-SYNUCLEIN Beclin1 

分 类 号：R742.5[医药卫生—神经病学与精神病学]