Amelioration of nerve demyelination by hydrogen-producing silicon-based agent in neuropathic pain rats

神经病理性疼痛 小胶质细胞 三叉神经节 医学 神经炎症 神经科学 三叉神经 上睑下垂 炎症体 炎症 发病机制 药理学 病理 免疫学 麻醉 生物 感觉系统
作者
Guo Mu,Qiang Li,Bin Lu,Xuan Yu
出处
期刊:International Immunopharmacology [Elsevier BV]
卷期号:117: 110033-110033 被引量:10
标识
DOI:10.1016/j.intimp.2023.110033
摘要

Trigeminal neuralgia (TN) is a complex orofacial neuropathic pain. The crippling condition's underlying mechanism is still not completely understood. The main cause of lightning-like pain in patients with TN may be chronic inflammation that causes nerve demyelination. Nano-silicon (Si) can safely and continuously produce hydrogen in the alkaline environment of the intestine to exert systemic anti-inflammatory effects. Hydrogen has a promising anti-neuroinflammatory impact. The study aimed to determine how intra-intestinal application of a hydrogen-producing Si-based agent affected the demyelination of the trigeminal ganglion in TN rats. We discovered that increased expression of the NLRP3 inflammasome and inflammatory cell infiltration occurred concurrently with demyelination of the trigeminal ganglion in TN rats. We could determine that the neural effect of the hydrogen-producing Si-based agent was connected to the inhibition of microglial pyroptosis by using transmission electron microscopy. The results demonstrated that the Si-based agent reduced the infiltration of inflammatory cells and the degree of neural demyelination. In a subsequent study, it was discovered that hydrogen produced by a Si-based agent regulates the pyroptosis of microglia may through the NLRP3-caspase-1-GSDMD pathway, preventing the development of chronic neuroinflammation and consequently lowering the incidence of nerve demyelination. This study offers a novel strategy for elucidating the pathogenesis of TN and developing potential therapeutic drugs.
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