Spinal cord injury can cause paralysis? ! NMN as a new target of spinal cord injury was found by "Shuiling Ling"...
Spinal cord injury (SCI) is a central nervous system disease with a high rate of paralysis.
With advances in regenerative medicine and neuroprotection research, scientists are always looking for new treatments.
A breakthrough study by a team from Capital Medical University has found that niacinamide mononucleotide (NMN), a precursor of NAD+, shows significant neuroprotective effects in a mouse model of spinal cord injury.
Figure 1. Protective effect of NMN on spinal cord injury
NMN restores NAD+ levels after spinal cord injury
The study found that NAD+ levels were significantly reduced after spinal cord injury, and supplementation with NMN could significantly restore this level.
NAD+ is a key molecule in cell energy metabolism and cell survival, and the recovery of its levels may be related to changes in the levels of NAD+ dependent enzymes.
Through RNA sequencing screening, the researchers found that the expression levels of two NAD+ dependent enzymes, heme oxygenase-1 (Hmox-1) and silencing information regulator 2 (SIRT2), were significantly different in different groups.
These findings suggest that NMN may influence the activity of these key enzymes by regulating NAD+ levels, thereby playing a neuroprotective role after spinal cord injury.
NMN promotes motor function recovery and pain relief
NMN supplementation not only restored NAD+ levels, but also significantly promoted the recovery of motor function after spinal cord injury in mice.
Through the BMS score, the researchers found that the motor function score of the NMN treated group was significantly higher than that of the control group.
NMN also significantly relieved pain caused by spinal cord injury.
Using Von-Frey mechanical pain threshold and thermal pain threshold tests, the researchers found that the pain response was significantly reduced in the NMN-treated mice.
NMN regulates gene expression to inhibit inflammatory response
The results showed that NMN could inhibit the inflammatory response.
This may be achieved by modulating signaling pathways, including pathways such as tumor necrosis factor.
By analyzing the interactions between proteins, the researchers found that after NMN treatment, inflammation-related factors such as IL-1β and IRF7 showed significant changes.
To further validate these findings, the researchers used quantitative reverse transcription polymerase chain reaction (QRPCR) and confirmed that NMN can indeed inhibit the expression of inflammatory factors such as IL-1β, TNF-α, IL-17A, IRF7, and chemokines (such as Cxcl10) in mice after spinal cord injury. These results suggest that NMN has potential in inflammation caused by mild spinal cord injury.
Sum up
The reduction in NAD+ levels after spinal cord injury can be compensated by NMN supplementation, which significantly restores motor function and reliefs pain in mouse models.
By down-regulating the expression of inflammatory factors and chemokines, NMN affects the inflammation-related signaling pathway and shows protective effect on the mouse model of spinal cord injury.
These findings provide new strategies and targets for the treatment of spinal cord injury and lay a foundation for future clinical applications.
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