ArticleCNS neuroscience & therapeutics2026
Sodium Butyrate Attenuates Sevoflurane-Induced Impaired Myelination and Neurobehavioral Deficits in Neonatal Mice via the H3K9ac/BDNF/TrkB Pathway.
Article in CNS neuroscience & therapeutics, 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
backgroundEarly-life exposure to sevoflurane is considered an important risk factor for abnormal neurodevelopment and may lead to impaired myelination and neurobehavioral deficits in neonatal mice. Sodium butyrate (NaB), a short-chain fatty acid (SCFA) with epigenetic regulatory activity, has shown neuroprotective effects in various neurological disorders. However, the role of NaB in sevoflurane-induced myelination impairment and the underlying molecular mechanisms remain unclear.
methodsAn in vivo neonatal mouse model of sevoflurane exposure was established to investigate its effects on myelination and neurobehavioral function. NaB intervention was then administered to evaluate its potential to ameliorate sevoflurane-induced myelination impairment and neurobehavioral deficits. In vitro, human oligodendrocyte precursor cells (HOPCs) were directly treated with different concentrations of NaB to examine its effects on cell proliferation, migration, differentiation, and related molecular signaling pathways.
resultsRepeated exposure to sevoflurane during the critical period of brain development in neonatal mice inhibited the proliferation and differentiation of oligodendrocyte precursor cells (OPCs), impaired myelination, and led to neurobehavioral deficits. NaB intervention ameliorated sevoflurane-induced myelination impairment and neurobehavioral dysfunction by regulating histone H3 lysine 9 acetylation (H3K9ac), upregulating brain-derived neurotrophic factor (BDNF) expression, promoting tropomyosin receptor kinase B (TrkB) phosphorylation, and increasing phosphorylated TrkB (p-TrkB) levels.
conclusionsRepeated sevoflurane exposure in neonatal mice inhibited OPC proliferation and differentiation, impaired myelination, and caused neurobehavioral deficits. NaB ameliorated these impairments by regulating H3K9ac modification and increasing BDNF and p-TrkB levels.
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