Background

Recent studies have demonstrated that nicotine exhibited anti-inflammatory and neuroprotective properties by interacting with the alpha 7 nicotinic acetylcholine receptor (α7nAChR). However, the role of nicotine in regeneration during peripheral nerve injury has not been elucidated. The aim of this study was to investigate whether nicotine down-regulated production of proinflammatory cytokines and promoted peripheral nerve regeneration in rats.

Methods

Rats challenged with sciatic nerve crush injury were treated with nicotine (1.5 mg/kg), three times per day. The expression of the proinflammatory cytokines tumor necrosis factor alpha (TNF-α) and interleukin (IL-1β), pinch test results, growth-associated protein 43 (GAP-43) expression, morphometric analyses, and the sciatic functional indexes were determined in sciatic nerves.

Results

Treatment with nicotine decreased local levels of TNF-α and IL-1β, and increased the expression of GAP-43. Nicotine also improved nerve regeneration and functional recovery. The overall protective effects of nicotine were reversed by concomitant treatment with α7nACHR antagonist methyllycaconitine, indicating that nicotine exerted its specific anti-inflammatory and neuroprotective effects through the α7nAChR.

Conclusion

These findings show that nicotine administration can provide a potential therapeutic pathway for the treatment of peripheral nerve injury, by a direct protective effect through the α7nAChR-mediated cholinergic anti-inflammatory pathway.

中文翻译：

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尼古丁通过减轻大鼠坐骨神经挤压伤后局部炎症性细胞因子的产生来发挥神经保护作用。

背景

最近的研究表明，尼古丁通过与α7烟碱型乙酰胆碱受体（α7nAChR）相互作用表现出抗炎和神经保护特性。然而，尚未阐明尼古丁在周围神经损伤期间再生中的作用。这项研究的目的是调查尼古丁是否下调了大鼠促炎细胞因子的产生并促进了周围神经的再生。

方法

坐骨神经挤压伤攻击的大鼠每天接受尼古丁（1.5 mg / kg）治疗3次。确定了促炎细胞因子肿瘤坏死因子α（TNF-α）和白细胞介素（IL-1β）的表达，捏试验结果，生长相关蛋白43（GAP-43）表达，形态分析和坐骨神经功能指数。坐骨神经。

结果

尼古丁治疗降低了TNF-α和IL-1β的局部水平，并增加了GAP-43的表达。尼古丁还改善了神经再生和功能恢复。尼古丁的总体保护作用通过与α7nACHR拮抗剂甲基甘可耐碱同时治疗而逆转，表明尼古丁通过α7nAChR发挥其特定的抗炎和神经保护作用。

结论

这些发现表明，通过α7nAChR介导的胆碱能抗炎途径的直接保护作用，尼古丁给药可以为周围神经损伤的治疗提供潜在的治疗途径。