ArticleJournal of neuroinflammation2017
The potential neuroprotective role of a histone deacetylase inhibitor, sodium butyrate, after neonatal hypoxia-ischemia.
Article in Journal of neuroinflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 2 of them syntheses that pooled it.
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Who cites it
49 citing papers in PubMed, 2 syntheses or guidelines pooled it, 107 citations in OpenAlex.
- Role and Mechanism of Microglia in White Matter Injury Recovery in Ischemic Stroke.Immunity, inflammation and disease · 2025Pooled it
- Postnatal Nutrition to Improve Brain Development in the Preterm Infant: A Systematic Review From Bench to Bedside.Frontiers in physiology · 2019Pooled it
- Magnesium Sulfate in Neonatal Hypoxic-Ischemic Encephalopathy: Bridging the Gap Between Molecular Neuroprotection and Clinical Outcomes.Current issues in molecular biology · 2026Review
- Gut microbiota-mediated neuroinflammation following stroke: mechanisms and intervention strategies.Journal of translational medicine · 2026Review
- An Epigenetic Switch for Sex-Specific Brain Resilience in Stroke: Targeting HDAC2 to Amplify Endogenous Oxytocin Signaling.ACS central science · 2026Article
- The Diverse Effect of HDAC Inhibitors: Sodium Butyrate and Givinostat on Microglia Polarization After Hypoxia-Ischemia In Vitro.International journal of molecular sciences · 2026Article
- Umbilical Cord Blood Endothelial Progenitor Cells Modulate Neurovascular Unit Damage in a Neonatal Rat Model of Hypoxia Ischemia.Stem cell reviews and reports · 2025Article
- Does the Maternal Gut Microbiome Influence the Outcome of Perinatal Asphyxia?Antioxidants (Basel, Switzerland) · 2025Review
- The Impact of the Histone Deacetylase Inhibitor-Sodium Butyrate on Complement-Mediated Synapse Loss in a Rat Model of Neonatal Hypoxia-Ischemia.Molecular neurobiology · 2025Article
- Effects and mechanisms of breastmilk stem cells in the treatment of white matter injury in newborn rats.Stem cell research & therapy · 2025Article
- Sodium butyrate attenuates microglia-mediated neuroinflammation by modulating the TLR4/MyD88/NF-κB pathway and microbiome-gut-brain axis in cardiac arrest mice.Molecular brain · 2025Article
- Oligodendrocyte progenitor cells' fate after neonatal asphyxia-Puzzling implications for the development of hypoxic-ischemic encephalopathy.Brain pathology (Zurich, Switzerland) · 2024Article
- CXCL10 is a crucial chemoattractant for efficient intranasal delivery of mesenchymal stem cells to the neonatal hypoxic-ischemic brain.Stem cell research & therapy · 2024Article
- Navigating the metabolic maze: anomalies in fatty acid and cholesterol processes in Alzheimer's astrocytes.Alzheimer's research & therapy · 2024Review
- Review
- The gut-brain-metabolic axis: exploring the role of microbiota in insulin resistance and cognitive function.Frontiers in microbiology · 2024Review
- Microbiota-derived short chain fatty acids in pediatric health and diseases: from gut development to neuroprotection.Frontiers in microbiology · 2024Review
- LOX-1 mediates inflammatory activation of microglial cells through the p38-MAPK/NF-κB pathways under hypoxic-ischemic conditions.Cell communication and signaling : CCS · 2023Article
- Vascular Stem Cells and the Role of B-Raf Kinase in Survival, Proliferation, and Apoptosis.International journal of molecular sciences · 2023Article
- The Bridge Between Ischemic Stroke and Gut Microbes: Short-Chain Fatty Acids.Cellular and molecular neurobiology · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHistone deacetylase inhibitor (HDACi), sodium butyrate (SB), has been shown to be neuroprotective in adult brain injury models. Potential explanation for the inhibitor action involves among others reduced inflammation. We therefore anticipated that SB will provide a suitable option for brain injury in immature animals. The aim of our study was to test the hypothesis that one of the mechanisms of protection afforded by SB after neonatal hypoxia-ischemia is associated with anti-inflammatory action. We examined the effect of SB on the production of inflammatory factors including analysis of the microglial and astrocytic cell response. We also examined the effect of SB on molecular mediators that are crucial for inducing cerebral damage after ischemia (transcription factors, HSP70, as well as pro- and anti-apoptotic proteins).
methodsSeven-day-old rat pups were subjected to unilateral carotid artery ligation followed by 60 min of hypoxia (7.6% O
resultsSB treatment-reduced brain damage, as assessed by HE staining, suppressed the production of inflammatory markers-IL-1β, chemokine CXCL10, and blocked ischemia-elicited upregulation of COX-2 in the damaged ipsilateral hemisphere. Furthermore, administration of SB promoted the conversion of microglia phenotype from inflammatory M1 to anti-inflammatory M2. None of the investigated molecular mediators that are known to be affected by HDACis in adults were modified after SB administration.
conclusionsAdministration of SB is neuroprotective in neonatal hypoxia-ischemia injury. This neuroprotective activity prevented the delayed rise in chemokine CXCL10, IL-1β, and COX-2 in the ipsilateral hemisphere. SB appears to exert a beneficial effect via suppression of HI-induced cerebral inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.