Objective: To investigate the role of 1-methyl-4-pehnyl-pyridine(MPP⁺) regulated mitochondrial autophagy in the pathogenesis 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 transfected with EGFP-LC3 and RFP-MITO.Expression of LAMP2A,Beclin1 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,Beclin1 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.