Nicotine Regulates LPS‐Induced Inflammatory Responses in HMC3 Microglia and Exerts Neuronal Protection
Yuhan Qin, Xiaohui Yan, Yanbo Luo, Hongjuan Wang, Yushan Tian, Xiaqing Wu, Huan Chen, Hongwei Hou, Qingyuan Hu
TL;DR
Nicotine reduces inflammation in microglia cells and protects neurons by activating a specific receptor, potentially offering new therapeutic approaches.
Contribution
This study reveals nicotine's anti-inflammatory and neuroprotective effects via α7 nAChR activation in microglia.
Findings
Nicotine inhibits LPS-induced inflammation in HMC3 microglia.
Nicotine promotes neurotrophic factor release and neuronal survival through α7 nAChR activation.
The anti-inflammatory effects involve increased PI3K phosphorylation.
Abstract
Microglia‐mediated neuroimmune responses have been implicated in central nervous system injury and disease pathogenesis. The α7 nicotinic acetylcholine receptor (α7 nAChR), which is expressed on microglia and participates in microenvironment interactions, is a key mediator of the cholinergic anti‐inflammatory pathway. Nicotine activates the α7 nAChR, which may mediate the inflammation of microglia. This study aims to explore the modulatory effects of nicotine on neuroinflammation and its potential indirect neuroprotective effects using an in vitro microglial cell inflammation model. In our study, inflammatory phenotype indicators and molecular mechanisms of HMC3 cells were analyzed. Furthermore, an HMC3 microglia‐SH‐SY5Y neuronal coculture system was constructed to investigate the indirect neuroprotective effects of nicotine. The results demonstrated that nicotine exerted an inhibitory…
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Taxonomy
TopicsNicotinic Acetylcholine Receptors Study · Vagus Nerve Stimulation Research · Neuroinflammation and Neurodegeneration Mechanisms