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

Front. Cell. Neurosci., 2023 · DOI: 10.3389/fncel.2023.1323566 · Published: December 14, 2023

Simple Explanation

This research investigates how nicotinamide mononucleotide (NMN) affects spinal cord injury (SCI) in mice. NMN is a substance that can be converted into nicotinamide adenine dinucleotide (NAD+), which is important for cell energy and survival. The study found that NMN supplementation after SCI helped restore NAD+ levels, improve motor function, and reduce pain in mice. This suggests NMN could have a protective effect on nerve cells and tissues damaged by SCI. The researchers used advanced techniques like RNA sequencing to analyze gene expression and identify the molecular mechanisms involved. They discovered that NMN can reduce inflammation and regulate several signaling pathways related to nerve regeneration and protection.

Study Duration

7 days

Participants

24 adult female C57BL/6N mice

Evidence Level

Level 1: Experimental study using a moderate-to-severe model of SCI by contusion in mice

Key Findings

1
NMN supplementation restores NAD+ levels after SCI, promoted motor function recovery, and alleviated pain in a mouse model.
2
RNA sequencing revealed that NMN can inhibit inflammation and potentially regulate signaling pathways, including interleukin-17 (IL-17), tumor necrosis factor (TNF), toll-like receptor, nod-like receptor, and chemokine signaling pathways.
3
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.

Research Summary

This study investigated the neuroprotective effects of nicotinamide mononucleotide (NMN) on spinal cord injury (SCI) in mice using RNA sequencing and qRT-PCR analysis. The results demonstrated that NMN supplementation can restore motor function and relieve pain after SCI, potentially by modulating inflammation-related signaling pathways. The study identifies key genes and pathways, such as IL-1β, IRF-7, Cxcl10, and the IL-17, TNF, and NOD-like receptor pathways, through which NMN exerts its neuroprotective effects.

Practical Implications

Therapeutic Potential

NMN may represent a potential therapeutic candidate for spinal cord injury by reducing the inflammatory response and promoting nerve regeneration.

Drug Development

Further research into the specific molecular mechanisms of NMN could lead to the development of targeted therapies for SCI.

Clinical Translation

Understanding the pathways and genes affected by NMN could aid in the clinical diagnosis and prognosis of SCI, as well as the development of practice guidelines.

Study Limitations

1
The study was conducted on mice, and results may not directly translate to humans.
2
Further research is needed to elucidate the specific molecular mechanisms by which NMN exerts its neuroprotective effects.
3
The study focused on a specific time point (7 days after injury), and longer-term effects of NMN need to be investigated.

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