NAD + affects differentially expressed genes- MBOAT2 - SLC25A21 - SOX6 in experimental autoimmune encephalomyelitis model.

Background: Nicotinamide adenine dinucleotide (NAD + ) plays a key role in neuroinflammation and neurodegeneration and provides anti-inflammatory and neuroprotective effects in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). Aim: In this study, we aimed to investigate whether NAD + affects differentially expressed genes (DEGs) in splenocytes of EAE mice to reveal candidate genes for the pathogenesis of MS. Methods: The EAE model was used to perform an intervention on NAD + to investigate its potential as a protective agent in inflammation and demyelination. Transcriptome analysis of nerve tissue was carried out to gain better insights into NAD + function. Effects of NAD + on DEGs in the splenocytes of EAE mice were investigated to determine its anti-inflammatory effect. Results: NAD + in EAE mice showed the clinical score was significantly improved (EAE 3.190 ± 0.473 vs. NAD + 2.049 ± 0.715). DEGs ( MBOAT2 , SLC25A21 , and SOX6 ) between the EAE and the EAE + NAD + groups showed that SOX6 was significantly improved after NAD + treatment compared with the EAE group, and other indicators were improved but did not reach statistical significance. NAD + exhibited clinical scores in EAE mice, and key inflammation was ameliorated in EAE mice spleen after NAD + intervention, while transcriptome analysis between EAE and EAE + NAD + groups showed several DEGs in the underlying mechanism. Conclusion: NAD + on DEGs attenuates disease severity in EAE. Transcriptome analysis on nerve tissue reveals several protein targets in the underlying mechanisms. However, NAD + does not significantly improve DEGs in the splenocytes of the EAE model.