国际神经病学神经外科学杂志2012,Vol.39Issue(6):489-493,5.
1-甲基-4-苯基吡啶离子调控线粒体自噬对线粒体氧化应激损伤的影响
Effect of 1-methyl-4-pehnyl-pyridine regulated mitochondrial autophagy on mitochondrial oxidative stress injury
摘要
Abstract
Objective To investigate the role of 1 -methyl-4-pehnyl -pyridine ( MPP+ ) regulated mitochondrial autophagy in the patho-genesis of Parkinson' s disease. Methods Human neuroblastoma cell lines (SH-SY5Y) were treated with MPP+ (0, 1 or 2 mmol/L) for 48 hrs and then were transfeeted with EGFP-LC3 and RFP-MITO. Expression of LAMP2A, Beclinl and LC3-II/LC-I proteins in SH-SY5Y cells was detected by Western blot after MPP+ treatment for 48 hrs. Cellular immunefluorescent chemical method was used to observe the change of autophagic vacuolization and the signals of EGFP-LC3 and RFP-MITO, and their subcellular colocalization. The flow cytometry was used to detect the mitochondrial membrane potential and reactive oxygen species content. Results The gray values of LAMP2A, Beclinl and LC3-II/LC3-I in the 1 mmol/L and 2 mmol/L MPP+ treatment groups were significantly increased compared with the control group (0 mmol/L MPP+ treat-ment) (P<0.05). The autophagy levels increased, the number of autophagic vacuolization increased, and expression of exogenous LC3 increased significantly in the two MPP+ treatment groups compared with the control group. EGFP-LC3 and RFP-MITO subcellular colocalization was observed in the MPP+ treatment groups. Mitochondrial reactive oxygen increased and mitochondrial membrane potential decreased significantly in the two MPP+ treatment groups compared with the control group. Conclusions MPP + can induce mitochondrial oxidative stress injury through regulating levels of mitochondrial autophagy.关键词
帕金森病/1-甲基-4-苯基吡啶离子/线粒体自噬/氧化应激/线粒体功能障碍Key words
Parkinson's disease/ l-methyl-4-pehnyl-pyridine/ mitochondrial autophagy/ oxidative stress/ mitochondrial dysfunction引用本文复制引用
马耀华,王雪晶,荆婧,马明明,杨期东,唐北沙,滕军放..1-甲基-4-苯基吡啶离子调控线粒体自噬对线粒体氧化应激损伤的影响[J].国际神经病学神经外科学杂志,2012,39(6):489-493,5.基金项目
国家自然科学基金(81241046 ()
81100949) ()