N-Acetyl Cysteine Protects against Methamphetamine-Induced Dopaminergic Neurodegeneration via Modulation of Redox Status and Autophagy in Dopaminergic Cells
Figure 1
MA induces autophagy. (A) Representative phase contrast microscopy pictures showing abundant cytoplasmic vacuoles (arrows) in N27 dopaminergic cells treated with MA (2 mM) for 12 hours. (B) Representative transmission electron microscopy image analysis of N27 dopaminergic cells exposed to MA (2 mM) for 12 hours: (a) untreated N27 dopaminergic cells; (b) boxed area; (c) autophagosomes observed in N27 dopaminergic cells treated with MA (2 mM) (arrows). Morphology of autophagosomes is characterized by the formation of double membrane vacuoles harboring damaged organelles (arrows) and insoluble protein aggregates. (C) Time-dependent increase in LC3-II levels. N27 dopaminergic cells were exposed to MA (2 mM) for 3, 6, 12, 18, and 24 hours. Equal loading of protein in each lane is confirmed by probing the membrane with β-actin antibody. Densitometry analysis of LC3-II induction is represented next to the Western blot image. LC3-II bands were quantified and expressed as percentage of untreated control. Data represent mean ± SEM, . ** and *** compared with untreated group.
