Regulation of LPS-Induced Inflammatory Responses in HMC3 Microglia by Nicotine and its Neuroprotective Effects

Abstract

Abstract Microglia-mediated neuroimmune responses have been implicated in CNS injury and disease pathogenesis. The α7 nicotinic acetylcholine receptor is one of the receptors that microglia interact with in the surrounding microenvironment. Nicotine, a tobacco-specific alkaloid, can activate the α7 nicotinic acetylcholine receptor, leading to immune modulation. The PI3K protein plays a critical role in regulating immune homeostasis in microglia and is particularly valuable in managing neuroinflammation. Moreover, the α7 nicotinic acetylcholine receptor seems to have a cascading regulatory effect on the PI3K protein, and nicotine may influence microglial inflammatory activity through this pathway. This article aims to explore the modulatory effects of nicotine on neuroinflammation and its potential indirect neuroprotective effects using an in vitro microglial cell inflammation model. The study demonstrated that nicotine had a modest inhibitory effect on the LPS-induced inflammation model of HMC3 microglia. It also increased the release of neurotrophic factors and improved neuronal survival by modifying the immune environment. The action of nicotine is considered to be primarily through the activation of α7 nAChR on HMC3 cells, leading to an increase in PI3K protein phosphorylation. This study sheds light on the immunomodulatory role of nicotine in the nervous system and serves as a valuable reference for uncovering the medicinal potential of nicotine.