Protective Effects Of Nicotinamide Mononucleotide Adenylate Transferase 1 (NMNAT1) On MES23.5 Parkinson 's Disease Cell Model

Objective To investigate the effects of gene overexpression and gene silening of nicotinamide mononucleotide adenylyltransferase (NMNAT1) on the length of axon, and the expression of Caspase3and SOD1in cell Models of Parkinson’s disease (PD) MES23.5cells.Methods Cells were divided into six groups:NMNAT1overexpression control group, NMNAT1overexpression negative group, NMNAT1overexpression positive group, NMNAT1siRNA control group, NMNAT1siRNA negative group, NMNAT1siRNA positive group. Before parkinsonian cell model establishmment, synthetic NMNAT1overexpression vehicle plasmids, NMNAT1overexpression plasmids, NMNAT1siRNA vehicle plasmids and NMNAT1siRNA plasmids were transfected into MES23.5cells using cell transfection techniques. The protein levels of Caspase3and SOD1in the six groups were measured by Western blots and axonal length was tested by Immunofluorescence.Results Compared with NMNAT1overexpression (siRNA) control group, marked increase in the protein level of Caspase3and decrease in SOD1and the axonal length was observed in NMNAT1overexpression (siRNA) negative group. Furthermore, Caspase3expression decreased and increased, SOD1expression increased and decreased, axoal length became longer and shorter respectively in NMNAT1overexpression positive group and in NMNAT1siRNA positive group, compared with NMNAT1overexpression (siRNA) negative group.Conclusion Our results suggest that cell apoptosis and oxidative stress plays a critical role in the pathogenesis of Parkinson disease. NMNAT1is effective to down-regulate the expression of Caspase3, up-regulate SOD1and delay axonal degeneration and it may, at least in part,provide a potential neuroprotective effect.