ArticleJournal of the American College of Surgeons2019
Valproic Acid and Neural Apoptosis, Inflammation, and Degeneration 30 Days after Traumatic Brain Injury, Hemorrhagic Shock, and Polytrauma in a Swine Model.
Article in Journal of the American College of Surgeons, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- 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
- Mood stabilizers and systemic inflammatory burden in euthymic patients with bipolar disorder: a comparative study of lithium and valproate.Psychopharmacology · 2026Article
- Valproic acid for treatment of traumatic brain injury: Study protocol for the VIBRANT prospective randomized trial.Transfusion · 2026Article
- Inflammatory cytokines as predictors of therapeutic response to valproate in patients with comorbid alcohol use disorder and bipolar disorder.Frontiers in psychiatry · 2026Article
- Histone Acetylation in Central and Peripheral Nervous System Injuries and Regeneration: Epigenetic Dynamics and Therapeutic Perspectives.International journal of molecular sciences · 2025Review
- A Combination of Low Doses of Lithium and Valproate Improves Cognitive Outcomes after Mild Traumatic Brain Injury.Journal of neurotrauma · 2025Article
- Emerging Neuroprotective Strategies: Unraveling the Potential of HDAC Inhibitors in Traumatic Brain Injury Management.Current neuropharmacology · 2024Review
- [A pilot study on the effects of early use of valproate sodium on neuroinflammation after traumatic brain injury].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2023Article
- Neuroinflammation and status epilepticus: a narrative review unraveling a complex interplay.Frontiers in pediatrics · 2023Review
- Innate immunity and immunotherapy for hemorrhagic shock.Frontiers in immunology · 2022Review
- Valproic Acid Reduces Neuroinflammation to Provide Retinal Ganglion Cell Neuroprotection in the Retina Axotomy Model.Frontiers in cell and developmental biology · 2022Article
- The Role of BDNF in Experimental and Clinical Traumatic Brain Injury.International journal of molecular sciences · 2021Review
- Valproic acid treatment rescues injured tissues after traumatic brain injury.The journal of trauma and acute care surgery · 2020Article
- Epigenetic Regulation of Ferroportin in Primary Cultures of the Rat Blood-Brain Barrier.Molecular neurobiology · 2020Article
- Druggable Transcriptional Networks in the Human Neurogenic Epigenome.Pharmacological reviews · 2019Review
- Annexin A1 Bioactive Peptide Promotes Resolution of Neuroinflammation in a Rat Model of Exsanguinating Cardiac Arrest Treated by Emergency Preservation and Resuscitation.Frontiers in neuroscience · 2019Article
- Safety and Outcomes of Valproic Acid in Subarachnoid Hemorrhage Patients: A Retrospective Study.Clinical neuropharmacologyArticle
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundA single-dose (150 mg/kg) of valproic acid (VPA) has been shown to decrease brain lesion size and improve neurologic recovery in preclinical models of traumatic brain injury (TBI). However, the longer-term (30 days) impact of single-dose VPA treatment after TBI has not been well evaluated. STUDY
designYorkshire swine were subjected to TBI (cortical impact), hemorrhagic shock, and polytrauma. Animals remained in hypovolemic shock for 2 hours before resuscitation with normal saline (NS; volume = 3× hemorrhaged volume) or NS + VPA (150 mg/kg) (n = 5/cohort). Brain samples were harvested 30 days after injuries. The cerebral cortex adjacent to the site of cortical impact was evaluated using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, immunohistochemistry, and Western blot analysis. Neural apoptosis, inflammation, degeneration, plasticity, and signaling pathways were evaluated.
resultsFor apoptosis, VPA treatment significantly decreased (p < 0.05) the number of TUNEL (+) cells and expression of cleaved-caspase 3. For inflammation and degeneration, expression of ionized calcium binding adaptor molecule-1, glial fibrillary acid protein, amyloid-β, and phosphorylated-Tau protein were significantly attenuated (p < 0.05) in the VPA-treated animals compared with the NS group. For, plasticity, VPA treatment also increased expression of brain-derived neurotrophic factor significantly (p < 0.05) compared with the NS group. For signaling pathways, nuclear factor-κB was decreased significantly (p < 0.05) and cytosolic IκBα expression was increased significantly (p < 0.05) in the VPA-treated animals compared with the NS group.
conclusionsAdministration of a single dose of VPA (150 mg/kg) can decrease neural apoptosis, inflammation, and degenerative changes, and promote neural plasticity at 30 days after TBI. In addition, VPA acts, in part, via regulation of nuclear factor-κB and IκBα pathways.
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