Roles of NAD in Protection of Axon against Degeneration via SIRT1 Pathways.

Axonal degeneration is a common pathological change of neurogenical disease which often arises before the neuron death. But it had not found any effective method to protect axon from degeneration. In this study we intended to confirm the protective effect of nicotinamide adenine dinucleotide (NAD), investigate the optimal administration dosage and time of NAD, and identify the relationship between silence signal regulating factor 1 (SIRT1) and axonal degeneration. An axonal degeneration model was established using dorsal root ganglion (DRG) neurons injured by vincristine to observe the protective effects of NAD to the injured axons. In addition, the potential contribution of the SIRT1 in axonal degeneration was also investigated. Through the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, immunochemistry staining, axons counting and length measuring, transmission electron microscope (TEM) observation, we demonstrated that NAD played an important role in preventing axonal degeneration. Further study revealed that the expression of SIRT1 and phosphorylated Akt1 (p-Akt1) was up-regulated when NAD was added into the culturing medium. Taking together, our results demonstrated that NAD might delay the axonal degeneration through SIRT1/Akt1 pathways.

Survival and differentiation of neuroepithelial stem cells on chitosan bicomponent fibers.

Chitosan is a popular biomaterial used in tissue engineering. Fibers of chitosan could provide a favorable anatomical substrate for cell growth which provides a promising application for axonal regeneration during peripheral injury. Neuroepithelial stem cells (NEPs) are the most primitive neural stem cells with multipotential for neuronal and glia differentiation. To assess the biocompatibility between NEPs and chitosan fibers, and to explore whether the NEPs have the ability to differentiation on chitosan fibers, NEPs were harvested from the neural tube and seeded on chitosan fibers in in vitro culture. The biocompatibility of chitosan fibers was tested by MTT assays. The growth and survival were observed by light and scanning electronic microscope at different times in culture. And, the differentiation of NEPs was examined by immunocytochemical staining. The results indicated that NEPs could grow on the chitosan fibers and attach firmly to the surface of fibers. On chitosan fibers, NEPs could differentiate into neurons and glia. Our study demonstrated that chitasan fibers had a good biocompatibility with NEPs which affords a potential alternative for the repair of peripheral nerve injury.