AUTHOR=Zhang Chunjia , Li Yan , Bai Fan , Talifu Zuliyaer , Ke Han , Xu Xin , Li Zehui , Liu Wubo , Pan Yunzhu , Gao Feng , Yang Degang , Wang Xiaoxin , Du Huayong , Guo Shuang , Gong Han , Du Liangjie , Yu Yan , Li Jianjun 

TITLE=The identification of new roles for nicotinamide mononucleotide after spinal cord injury in mice: an RNA-seq and global gene expression study

JOURNAL=Frontiers in Cellular Neuroscience

VOLUME=Volume 17 - 2023

YEAR=2023

URL=https://www.frontiersin.org/journals/cellular-neuroscience/articles/10.3389/fncel.2023.1323566

DOI=10.3389/fncel.2023.1323566

ISSN=1662-5102

ABSTRACT=Nicotinamide mononucleotide (NMN) serves as an important precursor to nicotinamide adenine dinucleotide (NAD+) and has been shown to provide neuroprotective effects in neurological diseases. In this study, a moderate-to-severe spinal cord injury (SCI) model was established in mice, and NMN treatment was administered immediately after injury for seven consecutive days. NMN supplementation restored NAD+ levels after SCI, promoted motor function recovery, and alleviated pain. This could potentially be associated with alterations in NAD+ dependent enzyme levels. RNA sequencing (RNA-seq) revealed that NMN can inhibit inflammation and potentially regulate signaling pathways, including interleukin-17 (IL-17), tumor necrosis factor (TNF), tolllike receptor, nod-like receptor, and chemokine signaling pathways. In addition, the construction of a protein-protein interaction (PPI) network and the screening of core genes showed that interleukin 1β (IL-1β), interferon regulatory factor 7 (IRF 7), C-X-C motif chemokine ligand 10 (Cxcl10), and other inflammation-related factors, changed significantly after NMN treatment. qRT-PCR confirmed the inhibitory effect of NMN on inflammatory factors (IL-1β, TNF-α, IL-17A, IRF7) and chemokines (chemokine ligand 3, Cxcl10) in mice following SCI. Our findings suggest that supplementation of NMN after SCI may be a potential strategy to improve inflammation response, alleviate pain, and restore motor function.