ArticlePharmacological reports : PR2026
GNE-317 ameliorates neuroinflammation stimulated by lipopolysaccharide via PI3K/Akt/mTOR pathway.
Article in Pharmacological reports : PR, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundMicroglial activation in the central nervous system plays a central role in neuroinflammation and contributes to the onset and progression of neurodegenerative diseases. This study aimed to evaluate the anti-inflammatory effects of GNE-317, a phosphoinositide 3-kinase/ mammalian target of rapamycin (PI3K/mTOR) inhibitor, in lipopolysaccharide (LPS)-induced neuroinflammatory models.
methodsBV2 microglial cells were stimulated with LPS, and the effects of GNE-317 were examined using Western blotting, quantitative real-time polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent assay (ELISA), nitric oxide (NO) assays, and immunofluorescence. For in vivo experiments, C57BL/6 mice received GNE-317 (25 mg/kg/day, intraperitoneal, ip) for three days, followed by LPS injection (5 mg/kg, ip). Microglial activation was assessed by anti-ionized calcium-binding adapter molecule-1 (IBA1) immunostaining in the brain.
resultsGNE-317 inhibited PI3K/protein kinase B (Akt)/mTOR signaling and reduced nuclear factor-kappa B (NF-κB) nuclear translocation in LPS-stimulated BV2 cells. It decreased inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) expression and lowered tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) production. In LPS-injected mice, GNE-317 reduced microglial activation in brain tissue.
conclusionsGNE-317 attenuates neuroinflammation by suppressing microglial activation through inhibition of the PI3K/Akt/mTOR and NF-κB pathways, supporting its potential as a therapeutic agent for microglia-mediated neuroinflammatory diseases.
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