@Article{ecn.2019.0426,
AUTHOR = {Dewei Wang, Tianyang Gao, Yingwei Zhao, Ye Mao, Zhigang Sheng, Qing Lan},
TITLE = {Nicotine exerts neuroprotective effects by attenuating local inflammatory cytokine production following crush injury to rat sciatic nerves},
JOURNAL = {European Cytokine Network},
VOLUME = {30},
YEAR = {2019},
NUMBER = {2},
PAGES = {59--66},
URL = {http://www.techscience.com/ECN/v30n2/65395},
ISSN = {1952-4005},
ABSTRACT = {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.},
DOI = {10.1684/ ecn.2019.0426}
}