ArticleOxidative medicine and cellular longevity2020
Valproate Sodium Protects Blood Brain Barrier Integrity in Intracerebral Hemorrhage Mice.
Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- The Role of Blood-Brain Barrier Disruption in Epilepsy: Mechanisms and Consequences.Neurology international · 2025Review
- Gestational Valproate Exposure Induces Tissue-Specific Transcriptomic Changes in the Neonatal Brain and Choroid Plexus in a Rat Model of Epilepsy, GAERS.The European journal of neuroscience · 2025Article
- Article
- Immune-mediated disruption of the blood-brain barrier after intracerebral hemorrhage: Insights and potential therapeutic targets.CNS neuroscience & therapeutics · 2024Review
- Article
- Valproate attenuates somatic hyperalgesia induced by orofacial inflammation combined with stress through inhibiting spinal IL-6 and STAT1 phosphorylation.Brain research bulletin · 2024Article
- Mechanisms of Blood-Brain Barrier Protection by Microbiota-Derived Short-Chain Fatty Acids.Cells · 2023Review
- Blood-brain barrier dysfunction in bipolar disorder: Molecular mechanisms and clinical implications.Brain, behavior, & immunity - health · 2022Review
- Dexmedetomidine post-conditioning protects blood-brain barrier integrity by modulating microglia/macrophage polarizationFrontiers in molecular neuroscience · 2022Article
- Diprotin A TFA Exerts Neurovascular Protection in Ischemic Cerebral Stroke.Frontiers in neuroscience · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Valproate sodium (VPA) is a traditional antiepileptic drug with a neuroprotective role in cerebrovascular disease. After intracerebral hemorrhage (ICH), mechanical compression by hematoma, neuroinflammation, oxidative stress, and cytotoxicity of hematoma lysates caused the destruction of the blood brain barrier (BBB). Targeting BBB is a major therapeutic method for patients with ICH. The purpose of the present study was to explore the role of VPA in preserving BBB integrity in the ICH model and investigate the underlying molecular mechanisms. One hundred and thirty-six adult male CD1 mice were randomly divided into five groups in the study. Mice subjected to ICH were administered intraperitoneally with VPA at 3, 24, and 48 h post-ICH, respectively. Neurobehavioral assessments, BBB permeability, Evans blue fluorescence, hematoma volume, and protein expression were evaluated. The administration of VPA reduced BBB permeability and improved the neurobehavior significantly post-ICH. VPA administration significantly decreased the expression of phosphorylated nuclear factor-kappa B (p-NF
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