Yachun Zheng, Jiaji Zhao, Shiquan Chang, Zifeng Zhuang, Si Waimei, Xin Li, Zenni Chen, Bei Jing, Di Zhang, Guoping Zhao
{"title":"β-谷甾醇通过抑制TLR4/NF-κB信号通路影响小胶质细胞极化减轻神经性疼痛。","authors":"Yachun Zheng, Jiaji Zhao, Shiquan Chang, Zifeng Zhuang, Si Waimei, Xin Li, Zenni Chen, Bei Jing, Di Zhang, Guoping Zhao","doi":"10.1007/s11481-023-10091-w","DOIUrl":null,"url":null,"abstract":"<p><p>The etiology of neuropathic pain is mostly caused by mechanical deformation and neuroinflammation, of which neuroinflammation is the main cause of chronic neuropathic pain. Activation of the TLR4/NF-κB signaling pathway mediates elevated levels of inflammatory cytokines, and we clearly demonstrated by in vivo and in vitro Western blot experiments that β-sitosterol significantly inhibited the elevated Toll-like receptor 4 (TLR4) expression levels and nuclear factor-kappa B (NF-κB) activation associated with inflammatory responses. In cellular experiments, we clearly saw that both β-sitosterol and TLR4/NF-κB signaling pathway inhibitors could inhibit M1 proinflammatory phenotype expression and promote M2 anti-inflammatory phenotype expression in GMI-R1 microglia by flow cytometry and immunofluorescence assays. Therefore, we suggest that β-sitosterol can affect microglial polarization by inhibiting the TLR4/NF-κB signaling pathway thereby reducing neuroinflammation and thus alleviating neuropathic pain.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":" ","pages":"690-703"},"PeriodicalIF":6.2000,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"β-Sitosterol Alleviates Neuropathic Pain by Affect Microglia Polarization through Inhibiting TLR4/NF-κB Signaling Pathway.\",\"authors\":\"Yachun Zheng, Jiaji Zhao, Shiquan Chang, Zifeng Zhuang, Si Waimei, Xin Li, Zenni Chen, Bei Jing, Di Zhang, Guoping Zhao\",\"doi\":\"10.1007/s11481-023-10091-w\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The etiology of neuropathic pain is mostly caused by mechanical deformation and neuroinflammation, of which neuroinflammation is the main cause of chronic neuropathic pain. Activation of the TLR4/NF-κB signaling pathway mediates elevated levels of inflammatory cytokines, and we clearly demonstrated by in vivo and in vitro Western blot experiments that β-sitosterol significantly inhibited the elevated Toll-like receptor 4 (TLR4) expression levels and nuclear factor-kappa B (NF-κB) activation associated with inflammatory responses. In cellular experiments, we clearly saw that both β-sitosterol and TLR4/NF-κB signaling pathway inhibitors could inhibit M1 proinflammatory phenotype expression and promote M2 anti-inflammatory phenotype expression in GMI-R1 microglia by flow cytometry and immunofluorescence assays. Therefore, we suggest that β-sitosterol can affect microglial polarization by inhibiting the TLR4/NF-κB signaling pathway thereby reducing neuroinflammation and thus alleviating neuropathic pain.</p>\",\"PeriodicalId\":73858,\"journal\":{\"name\":\"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology\",\"volume\":\" \",\"pages\":\"690-703\"},\"PeriodicalIF\":6.2000,\"publicationDate\":\"2023-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1007/s11481-023-10091-w\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2023/12/2 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/s11481-023-10091-w","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/12/2 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
β-Sitosterol Alleviates Neuropathic Pain by Affect Microglia Polarization through Inhibiting TLR4/NF-κB Signaling Pathway.
The etiology of neuropathic pain is mostly caused by mechanical deformation and neuroinflammation, of which neuroinflammation is the main cause of chronic neuropathic pain. Activation of the TLR4/NF-κB signaling pathway mediates elevated levels of inflammatory cytokines, and we clearly demonstrated by in vivo and in vitro Western blot experiments that β-sitosterol significantly inhibited the elevated Toll-like receptor 4 (TLR4) expression levels and nuclear factor-kappa B (NF-κB) activation associated with inflammatory responses. In cellular experiments, we clearly saw that both β-sitosterol and TLR4/NF-κB signaling pathway inhibitors could inhibit M1 proinflammatory phenotype expression and promote M2 anti-inflammatory phenotype expression in GMI-R1 microglia by flow cytometry and immunofluorescence assays. Therefore, we suggest that β-sitosterol can affect microglial polarization by inhibiting the TLR4/NF-κB signaling pathway thereby reducing neuroinflammation and thus alleviating neuropathic pain.