Aim: To
investigate the effect of N-acetylcysteine (NAC), a
potent antioxidant, on neuron differentiation of cultured mouse embryonic stem
cells (ESCs) induced by retinoic acid (RA) in
vitro. Superior cervical
ganglion (SCG) neurons were used to study the effect of NAC on neuritogenesis.
Methods: We obtained a high percentage of MAP2-positive neurons derived from embryoid bodies (EBs) induced by
RA by administering 1 mmol/L NAC at differentiation
day 0. On differentiation day 8,
the expression of MAP2 protein was strongly upregulated in the presence of NAC. NAC
promoted neuron differentiation of ES cells in a dose- and time-dependent
manner. Notably, NAC suppressed
cell death caused by RA during neuron differentiation. In addition, neurite extension of SCG neurons was greatly stimulated in the presence of NAC.
Results: During
both phases, nicotine increased motor activity across test days in a
dose-dependent manner. Motor
activity of rats treated with nicotine during adolescence was positively
correlated with the activity recorded from the same rats during adulthood. In both phases, there were profound
individual differences in the responses to the nicotine treatments. In addition, adolescent rats treated
with nicotine did not show decreased motor response to the initial exposure to
nicotine. Finally, adolescent
exposure to nicotine at 0.4 mg/kg, but not adulthood exposure to the same dose
of nicotine, produced a robust disruption of PPI, with individual rats showing
different degrees of PPI disruption.
Conclusion: These results show that NAC enhanced both neuron differentiation and neuritogenesis, suggesting that it may be used in the
development of novel therapeutic approaches targeting neuron loss and neurite dystrophy in neurodegenerative diseases.
|
