Abstract: To explore the effect of nicotinamide adenine dinucleotide (NAD) in delaying axonal degeneration. MethodsDorsal root ganglion(DRG) cells were isolated from neonate rats and cultured in DMEM/F12 medium, and then treated with vincristine to establish an axonal degeneration model. NAD of different concentrations was added in the culture medium to detect its protective effects. Axonal degeneration was identified by immunocytochemical staining and by MTT analysis, and length and number of DRG cells were determined using the software IPP. ResultsDRG cells treated with vincristine suffered typical axonal degeneration in the distal end of the axon at 8h in vitro. The axon was swollen and disrupted at 12?h. There was no intact axonal structure after a 24?htreatment with vincristine. The end of the axon had normal axonal structure at 12?h in culture, and the axon had light degeneration at 24?h in vitro culture. MTT analysis showed that the experimental groups containing NAD had higher cell survival rates than the injury groups. Axon counting showed that only 35% of axons degenerated in the experimental groups, while only 60% of axons degenerated in the injury groups. ConclusionNAD plays an important role in preventing axonal degeneration.

Key words: Axonal, Dorsal root ganglia, Nicotinamide adenine dinucleotide, Rat,Wistar