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 (, , and ) between the EAE and the EAE + NAD groups showed that 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.
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| http://dx.doi.org/10.1080/00207454.2024.2313022 | DOI Listing |
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