ArticleMolecular medicine (Cambridge, Mass.)2025
Evobrutinib mitigates neuroinflammation after ischemic stroke by targeting M1 microglial polarization via the TLR4/Myd88/NF-κB pathway.
Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed.
- Ptbp2 Alleviates Neuroinflammation and Blood-brain Barrier Disruption via Modulating Microglial Polarization in Ischemic Stroke.Molecular neurobiology · 2026Article
- Byakangelicol Alleviates Ischemic Brain Injury by Inhibiting Microglial Activation and Oxidative Stress.Molecular neurobiology · 2026Article
- Promising Potential of Edaravone-Loaded Nanogel in Ameliorating of Stroke in Rats: The Modulation of Immune Response.BioMed research international · 2026Article
- TLR4 mediates post-traumatic depression via kynurenine pathway activation in a murine traumatic brain injury model.Frontiers in pharmacology · 2026Article
- Calycosin attenuates LPS-induced microglia inflammatory responses and microglia-mediated synaptic impairment via modulation of TLR4/MyD88/NF-κB signaling pathway.Frontiers in pharmacology · 2026Article
- The mechanism of dynamic switching between M1/M2 phenotypes of microglia in neuropathic pain: a narrative review.Frontiers in molecular neuroscience · 2026Review
- Bimodal regulation and precision therapy of neutrophil extracellular traps in liver ischemia-reperfusion injury: recent advances.Frontiers in immunology · 2026Review
- Inflammation increases the penetrance of behavioral impairment inbioRxiv : the preprint server for biology · 2025Article
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14 authors.
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Abstract
backgroundEvobrutinib, a third-generation Bruton's tyrosine kinase (BTK) inhibitor, shows great promise for treating neuroinflammatory diseases due to its small molecular size, ease of absorption, and ability to cross the blood-brain barrier. Although previous studies have confirmed significant BTK expression in microglia, the potential of Evobrutinib to treat ischemic stroke by modulating microglial function and its underlying mechanisms remain to be elucidated.
methodsMale C57BL/6 mice with cerebral ischemia was established to evaluate the effects of oral Evobrutinib treatment. Assessments included TTC staining, behavioral experiments, and pathological examinations were used to evaluate cerebral ischemic injury. Western Blot, flow cytometry, and qPCR were employed to monitor changes in BTK and pBTK expression in microglia and the impact of Evobrutinib on neuroinflammation following the stroke. In vitro, primary microglia were generated to determine the effects of Evobrutinib on the TLR4/ Myd88/NF-κB pathway and on the polarization of microglial subtypes.
resultsThe expression of BTK and pBTK is upregulated in microglia under conditions of cerebral ischemia and oxygen-glucose deprivation (OGD). Evobrutinib treatment not only reduced infarct volume in mice but also ameliorated pathological damage and facilitated neurological function recovery. Flow cytometry revealed that Evobrutinib decreased inflammatory cell infiltration and promoted M2 microglia polarization post-stroke. In vitro studies demonstrated that Evobrutinib downregulated the proportion of pro-inflammatory microglia and curtailed the secretion of inflammatory factors under OGD conditions. Mechanistically, Evobrutinib attenuated the OGD-induced upregulation of TLR4/Myd88/NF-κB expression, an effect that was further enhanced by the addition of the TLR4 pathway inhibitor TAK242.
conclusionsEvobrutinib inhibits the expression and activation of BTK in microglia, reducing M1 microglia-mediated neuroinflammation and alleviating ischemic injury following stroke. This effect is mechanistically linked to the inhibition of TLR4/Myd88/NF-κB-mediated M1 polarization of microglia.
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