Acetylglutamine facilitates motor recovery and alleviates neuropathic pain after brachial plexus root avulsion in rats

Journal of Translational Medicine, 2023 · DOI: https://doi.org/10.1186/s12967-023-04399-7 · Published: August 1, 2023

Simple Explanation

This study investigates the potential of Acetylglutamine (NAG) to improve motor and sensory recovery in rats after brachial plexus root avulsion (BPRA), a severe nerve injury. BPRA leads to loss of upper limb motor function due to motoneuron death and muscle denervation. The researchers hypothesized that NAG, known for its neuroprotective and anti-inflammatory properties, could aid in recovery. They surgically induced BPRA in rats and then treated them with NAG or saline. The study found that NAG significantly improved motor function, reduced neuropathic pain, enhanced motoneuron survival, promoted axonal remyelination, and lessened muscle atrophy. These results suggest NAG could be a novel treatment for BPRA.

Study Duration

8 weeks

Participants

30 adult male Sprague Dawley (SD) rats

Evidence Level

Not specified

Key Findings

1
NAG significantly accelerated the recovery of motor function in the injured forelimbs of rats following BPRA, as evidenced by improved scores in grooming tests, cylinder tests, and food pellet-taking tests.
2
NAG treatment enhanced motoneuronal survival in the anterior horn of the spinal cord in rats following BPRA, as shown by Nissl staining and increased levels of GAP-43 and p-Akt, while reducing nNOS expression.
3
NAG treatment inhibited the expression of proinflammatory cytokines (IL-1β, IL-6, TNF-α, p-p65) and pyroptosis pathway proteins (NLRP3, GSDMD, caspase-1) in the spinal cord of rats following BPRA.

Research Summary

This study investigated the effects of acetylglutamine (NAG) on motor and sensory recovery after brachial plexus root avulsion (BPRA) in rats. BPRA leads to significant motor neuron death and loss of upper limb function. The results showed that NAG treatment significantly accelerated motor function recovery, enhanced motoneuron survival, inhibited proinflammatory cytokines and pyroptosis pathway factors, facilitated axonal remyelination, and alleviated biceps brachii atrophy. The conclusion is that NAG promotes functional motor recovery and alleviates neuropathic pain by enhancing motoneuron survival and axonal remyelination and inhibiting the pyroptosis pathway after BPRA in rats.

Practical Implications

Potential Novel Treatment for BPRA

NAG shows promise as a new therapeutic agent for brachial plexus root avulsion, addressing both motor deficits and neuropathic pain.

Clinical Applications

Given its neuroprotective and anti-inflammatory effects, NAG could be explored for treating other neurological conditions involving nerve injury and inflammation.

Further Research

Future studies should investigate the optimal dosage, administration route, and long-term effects of NAG in BPRA treatment, as well as its impact on motoneuron regeneration.

Study Limitations

1
The study was conducted on rats, and the results may not be directly translatable to humans.
2
Further studies are needed to investigate the effect of NAG on regeneration of motoneurons after BPRA.
3
The specific mechanisms by which NAG exerts its neuroprotective effects require further elucidation.

Your Feedback

Was this summary helpful?

Back to Regenerative Medicine