ArticleNeurochemical research2013
Class I histone deacetylase inhibitor valproic acid reverses cognitive deficits in a mouse model of septic encephalopathy.
Article in Neurochemical research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 3 of them syntheses that pooled it.
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Who cites it
42 citing papers in PubMed, 3 syntheses or guidelines pooled it, 77 citations in OpenAlex.
- What Animal Models Can Tell Us About Long-Term Psychiatric Symptoms in Sepsis Survivors: a Systematic Review.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Pooled it
- Systematic review and meta-analysis of experimental studies evaluating the organ protective effects of histone deacetylase inhibitors.Translational research : the journal of laboratory and clinical medicine · 2019Pooled it
- Long-Term Cognitive Outcomes After Sepsis: a Translational Systematic Review.Molecular neurobiology · 2019Pooled it
- Modulation of the cognitive impairment associated with Alzheimer's disease by valproic acid: possible drug repurposing.Inflammopharmacology · 2025Article
- Modulation of brain immune microenvironment and cellular dynamics in systemic inflammation.Theranostics · 2025Article
- Isoflurane-induced neuroinflammation and NKCC1/KCC2 dysregulation result in long-term cognitive disorder in neonatal mice.BMC anesthesiology · 2024Article
- Exploring Neuroprotective Agents for Sepsis-Associated Encephalopathy: A Comprehensive Review.International journal of molecular sciences · 2023Review
- Emodin Promotes Autophagy and Prevents Apoptosis in Sepsis-Associated Encephalopathy through Activating BDNF/TrkB Signaling.Pathobiology : journal of immunopathology, molecular and cellular biology · 2022Article
- A metabolite attenuates neuroinflammation, synaptic loss and cognitive deficits induced by chronic infection ofFrontiers in immunology · 2022Article
- Neuroimmune Regulation in Sepsis-Associated Encephalopathy: The Interaction Between the Brain and Peripheral Immunity.Frontiers in neurology · 2022Review
- β-Glucan from Lentinula edodes prevents cognitive impairments in high-fat diet-induced obese mice: involvement of colon-brain axis.Journal of translational medicine · 2021Article
- Valproic acid inhibits interferon-γ production by NK cells and increases susceptibility to Listeria monocytogenes infection.Scientific reports · 2020Article
- Ethyl pyruvate protects against sepsis-associated encephalopathy through inhibiting the NLRP3 inflammasome.Molecular medicine (Cambridge, Mass.) · 2020Article
- Article
- Dysregulation of BDNF/TrkB signaling mediated by NMDAR/CaJournal of neuroinflammation · 2020Article
- Curdlan Prevents the Cognitive Deficits Induced by a High-Fat Diet in Mice via the Gut-Brain Axis.Frontiers in neuroscience · 2020Article
- Disruption of Striatal-Enriched Protein Tyrosine Phosphatase Signaling Might Contribute to Memory Impairment in a Mouse Model of Sepsis-Associated Encephalopathy.Neurochemical research · 2019Article
- NLRP3/Caspase-1 Pathway-Induced Pyroptosis Mediated Cognitive Deficits in a Mouse Model of Sepsis-Associated Encephalopathy.Inflammation · 2019Article
- Histone Deacetylation Inhibitors as Therapy Concept in Sepsis.International journal of molecular sciences · 2019Review
- Systemic Inflammation Impairs Mood Function by Disrupting the Resting-State Functional Network in a Rat Animal Model Induced by Lipopolysaccharide Challenge.Mediators of inflammation · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence suggests that histone deacetylase inhibitor exert neuroprotective effects in animal models of neurological diseases. We investigated for the first time whether class I histone deacetylase inhibitor valproic acid (VPA) can reverse cognitive deficits in a mouse model of sepsis-associated encephalopathy (SAE). Moreover, the possible mechanisms of protection were also explored. A mouse model of SAE was induced in adult male mice by cecal ligation and puncture (CLP). Mice received an administration of saline or VPA (100 mg/kg) once daily for 14 consecutive days starting either immediately or 2 weeks after operation. Furthermore, the TrkB antagonist K252a was used in another group of experiment to investigate whether brain-derived neurotrophic factor (BDNF)-TrkB signaling pathway is involved in the protection of VPA. Our data suggested that CLP resulted in significant cognitive impairments accompanied by increased expressions in interleukin-1β and caspase-3, and decreased expressions in BDNF, phospho-TrkB (pTrkB), postsynaptic density 95, and synapses, which were reversed by VPA. However, TrkB antagonist K252a abolished the beneficial effects of VPA with regard to cognition and decreased pTrkB expression and synapses in the hippocampus. Taken together, the findings of the present study suggested chronic treatment with VPA reverses cognitive deficits through mechanisms probably via a reduction in inflammation and apoptosis in the brain, as well as the activation of the BDNF-TrkB signaling pathway in a mouse model of SAE.
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