ArticleJournal of neuroinflammation2016
The histone deacetylase inhibitor, sodium butyrate, exhibits neuroprotective effects for ischemic stroke in middle-aged female rats.
Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
89 citing papers in PubMed, 2 syntheses or guidelines pooled it, 144 citations in OpenAlex.
- Protective effects of butyrate on cerebral ischaemic injury in animal models: a systematic review and meta-analysis.Frontiers in neuroscience · 2024Pooled 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
- Epigenetic histone deacetylase inhibition by sodium butyrate reduces neuroinflammation, improves neurological dysfunction and promotes disease modification of epileptogenesis following traumatic brain injury.Experimental neurology · 2026Article
- Gut microbiota-mediated neuroinflammation following stroke: mechanisms and intervention strategies.Journal of translational medicine · 2026Review
- Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- Targeting epigenetic remodeling of the blood-brain barrier: current knowledge for drug therapy.Epigenomics · 2026Review
- Histone and non-histone (de)acetylation impact on the blood-brain barrier.Fluids and barriers of the CNS · 2026Review
- Sex differences in the effects of shift work-like schedules on gut microbiome and intestinal barrier in relation to stroke survival.PloS one · 2026Article
- Modulation of NF-κB pathway in cancer therapy by sodium butyrate and Isoproterenol.Molecular biology reports · 2025Review
- Does the Maternal Gut Microbiome Influence the Outcome of Perinatal Asphyxia?Antioxidants (Basel, Switzerland) · 2025Review
- Knockdown of ATF3 Alleviates Ischemic Stroke and Inhibits Ferroptosis via Activating the Keap1/Nrf2/HO- 1 Pathway.Molecular neurobiology · 2025Article
- Epigenetic Regulation in Ischemic Neuroprotection: The Dual Role of HDACs and HATs in Neuroinflammation and Recovery.Antioxidants (Basel, Switzerland) · 2025Review
- Post-stroke butyrate treatment shows sex-dependent microglial responses but does not improve outcomes in a mouse model of endothelin-1 sensory motor stroke.BMC neuroscience · 2025Article
- Sodium butyrate alleviates spinal cord injury via inhibition of NLRP3/Caspase-1/GSDMD-mediated pyroptosis.Metabolic brain disease · 2025Article
- Gastrointestinal Dysfunction and Dysbiosis in Ischemic Stroke: Opportunities for Therapeutic Intervention.Pharmaceuticals (Basel, Switzerland) · 2025Review
- 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
- Silencing ATF3 mediates mitochondrial homeostasis and improves ischemic stroke through regulating the MAPK signaling pathway.Frontiers in molecular neuroscience · 2025Article
- Ontogenetic Neuroimmune Changes Following Prenatal Alcohol Exposure: Implications for Neurobehavioral Function.Advances in experimental medicine and biology · 2025Review
- Potential therapeutic targets for ischemic stroke in pre-clinical studies: Epigenetic-modifying enzymes DNMT/TET and HAT/HDAC.Frontiers in pharmacology · 2025Review
- Effects of Short Chain Fatty Acid-Butyrate Supplementation on the Disease Severity, Inflammation, and Psychological Factors in Patients With Active Ulcerative Colitis: A Double-Blind Randomized Controlled Trial.Journal of nutrition and metabolism · 2025Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundSodium butyrate (NaB) is a histone deacetylase (HDAC) inhibitor exhibiting anti-inflammatory and neuroprotective effects in a rat ischemic model of stroke as well as a myocardial ischemia model. Although clinical evidence shows that older women are at higher risk for stroke occurrence and greater stroke severity, no studies have evaluated the effectiveness of NaB either in females or in older animals.
methodsTo determine the effects of NaB on stroke in older females, acyclic middle-aged Sprague-Dawley female rats (9-11 months old, constant diestrus) were subject to middle cerebral artery occlusion (MCAo) by intracerebral injection of recombinant endothelin-1. Rats were treated with NaB (300 mg/kg, i.p.) at 6 and 30 h following ET-1 injection. Animals were sacrificed at the early (2 days) or late (5 days) acute phase after MCAo. Serum and tissue lysates were collected for biochemical analyses.
resultsNaB treatment reduced infarct volume and ameliorated sensory motor impairment in middle-aged female rats, when measured at 2 and 5 days post MCAo. At the early acute phase (2 days post stroke), NaB treatment decreased brain lipid peroxides, and reduced serum levels of GFAP, a surrogate marker of blood-brain barrier (BBB) permeability. NaB also reduced expression of the inflammatory cytokine IL-1beta in circulation and IL-18 in the ischemic hemisphere. At the late acute phase (5 days post stroke), NaB treatment further suppressed MCAo-induced increase of IL-1beta, IL-17A, and IL-18 in brain lysates (cortex and striatum) from the ischemic hemisphere, and decreased ischemia-induced upregulation of IL-1beta and IL-18 in circulation, indicating a potent anti-inflammatory effect of the HDAC inhibitor. Moreover, NaB treatment also increased expression of IGF-1, a known neuroprotectant, in peripheral tissue including serum, liver, and spleen at the late acute phase.
conclusionsThese data provide the first evidence that delayed (>6 h) NaB treatment post-stroke is neuroprotective in older female rats. Additionally, these data also show that in addition to its well-known anti-inflammatory actions, NaB may exert a biphasic effect after stroke, operating initially to reduce BBB permeability and oxidative stress in the brain, and later, elevating IGF-1 expression in peripheral tissues.
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