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.
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http://dx.doi.org/10.1007/s11481-023-10091-w | DOI Listing |
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