Glycyrrhizic acid promote remyelination after peripheral nerve injury by reducing NF-κB activation

IF 2.5 4区 医学 Q3 NEUROSCIENCES Neuroscience Letters Pub Date : 2024-10-11 DOI:10.1016/j.neulet.2024.138009
Yuan Yue , Jing Wang , Jun Tian
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Abstract

Background

Peripheral nerve injury (PNI) causes motor and sensory defects, has strong impact on life quality and still has no effective therapy. Glycyrrhizic acid (GA) is one of the most widely used in traditional Chinese prescriptions and as a flavoring additive in the food industry; the aims of the study were to investigate the effects of GA during sciatic nerve regeneration in a mouse model of sciatic nerve crush injury.

Methods

We established peripheral nerve crush model and investigated the effects of GA. We further studied the potential mechanism of action of GA by Western blotting, fluorescence immunohistochemistry, and PCR analysis.

Results

GA improves the sensory and motor functions of crushed nerve by preventing Schwann cell loss, axonal loss and promoting remyelination of sciatic nerve. Affected by GA, the inflammatory response in the distal part of the sciatic nerve was reduced. Finally, the neuroprotective properties of GA may be regulated by the nuclear factor (NF)‐κB pathway.

Conclusions

Our data suggest that GA can effectively alleviate PNI, and the mechanism involves mediating inflammatory response by suppressing NF-κB pathway activation. Thus, GA may represent a potential therapeutic intervention for nerve crush injury.
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甘草酸通过减少 NF-κB 激活促进周围神经损伤后的再髓鞘化。
背景:周围神经损伤(PNI)会导致运动和感觉缺陷,对生活质量有很大影响,目前仍没有有效的治疗方法。本研究旨在探讨甘草酸在坐骨神经挤压伤小鼠模型中对坐骨神经再生的影响:方法:我们建立了坐骨神经挤压伤小鼠模型,并研究了 GA 的作用。结果:GA能改善小鼠坐骨神经的感觉和运动功能:结果:GA 通过防止许旺细胞丢失、轴突丢失和促进坐骨神经再髓鞘化,改善了粉碎神经的感觉和运动功能。受 GA 影响,坐骨神经远端部分的炎症反应有所减轻。最后,GA的神经保护特性可能受核因子(NF)-κB通路调控:我们的数据表明,GA 能有效缓解 PNI,其机制包括通过抑制 NF-κB 通路的激活来调解炎症反应。因此,GA 可能是治疗神经挤压伤的一种潜在干预措施。
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来源期刊
Neuroscience Letters
Neuroscience Letters 医学-神经科学
CiteScore
5.20
自引率
0.00%
发文量
408
审稿时长
50 days
期刊介绍: Neuroscience Letters is devoted to the rapid publication of short, high-quality papers of interest to the broad community of neuroscientists. Only papers which will make a significant addition to the literature in the field will be published. Papers in all areas of neuroscience - molecular, cellular, developmental, systems, behavioral and cognitive, as well as computational - will be considered for publication. Submission of laboratory investigations that shed light on disease mechanisms is encouraged. Special Issues, edited by Guest Editors to cover new and rapidly-moving areas, will include invited mini-reviews. Occasional mini-reviews in especially timely areas will be considered for publication, without invitation, outside of Special Issues; these un-solicited mini-reviews can be submitted without invitation but must be of very high quality. Clinical studies will also be published if they provide new information about organization or actions of the nervous system, or provide new insights into the neurobiology of disease. NSL does not publish case reports.
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