ArticleFrontiers in molecular neuroscience2018
Valproic Acid Attenuates Traumatic Brain Injury-Induced Inflammation
Article in Frontiers in molecular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 97 citations in OpenAlex.
- Post-translational modifications in Neuroimmune cells during neuroinflammation: integrated regulatory networks and therapeutic opportunities.Biology direct · 2026Review
- Retraction Note: Omega-3 polyunsaturated fatty acid attenuates traumatic brain injury-induced neuronal apoptosis by inducing autophagy through the upregulation of SIRT1-mediated deacetylation of Beclin-1.Journal of neuroinflammation · 2026Article
- HIPK2 protects neurons from oxidative stress and modulates central nervous system responses following traumatic brain injury.Iranian journal of basic medical sciences · 2026Article
- Valproic acid boosts hair follicle stem cell resilience to oxygen-glucose deprivation through autophagy induction and AKT/mTOR suppression.Scientific reports · 2025Article
- Histone Deacetylase 2 in Alzheimer's Disease: A Comprehensive Molecular Blueprint for Therapeutic Targeting.Molecular neurobiology · 2025Review
- Combination Therapy of Estrogen and Progesterone Attenuates Behavioral Impairments and Autophagy via circLrp1b/miR-27a-3p/Dram2 Pathway After Traumatic Brain Injury.Molecular neurobiology · 2025Article
- Xuebijing Promotes HMGB1-Mediated Autophagy to Alleviate Oxidative Stress and Inflammation in Heat Stroke-Induced Brain Damage.Molecular neurobiology · 2025Article
- OSBP Participates in Neural Damage Repair by Regulating Lysosome Transport Under Oxidative Stress.Molecular neurobiology · 2025Article
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- A Combination of Low Doses of Lithium and Valproate Improves Cognitive Outcomes after Mild Traumatic Brain Injury.Journal of neurotrauma · 2025Article
- Gut microbiota remodeling exacerbates neuroinflammation and cognitive dysfunction via the microbiota-gut-brain axis in prenatal VPA-exposed C57BL/6 mice offspring.Frontiers in immunology · 2025Article
- Inhibition of HDAC3 induces neuroprotection by activating the Npas4 signaling pathway following surgical brain injury in rats.Iranian journal of basic medical sciences · 2025Article
- Deferoxamine Induces Autophagy Following Traumatic Brain Injury via TREM2 on Microglia.Molecular neurobiology · 2024Article
- Microglial histone deacetylase 2 is dispensable for functional and histological outcomes in a mouse model of traumatic brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
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- Valproate attenuates somatic hyperalgesia induced by orofacial inflammation combined with stress through inhibiting spinal IL-6 and STAT1 phosphorylation.Brain research bulletin · 2024Article
- Emerging Neuroprotective Strategies: Unraveling the Potential of HDAC Inhibitors in Traumatic Brain Injury Management.Current neuropharmacology · 2024Review
- Baicalein Long-Circulating Liposomes Improve Histological and Functional Outcomes After Traumatic Brain Injury.Advances in pharmacological and pharmaceutical sciences · 2024Article
- Valproic acid and/or rapamycin preconditioning protects hair follicle stem cells from oxygen glucose serum deprivation-induced oxidative injury via activating Nrf2 pathway.Molecular biology research communications · 2024Article
- Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microglial activation and the inflammatory response in the central nervous system (CNS) play important roles in secondary damage after traumatic brain injury (TBI). Transcriptional activation of genes that limit secondary damage to the CNS are mediated by a cis-acting element called the antioxidant responsive element (ARE). ARE is known to associate with the transcription factor NF-E2-related factor 2 (Nrf2), a transcription factor that is associated with histone deacetylases (HDACs). This pathway, known as the Nrf2/ARE pathway, is a critical antioxidative factor pathway that regulates the balance of oxygen free radicals and the inflammatory response, and is also related to autophagic activities. Although valproic acid (VPA) is known to inhibit HDACs, it is unclear whether VPA plays a role in the microglia-mediated neuroinflammatory response after TBI via regulating oxidative stress and autophagy induced by the Nrf2/ARE signaling pathway. In this study, we demonstrate that microglial activation, oxidative stress, autophagy, and the Nrf2/ARE signaling pathway play essential roles in secondary injury following TBI. Treatment with VPA alleviated TBI-induced secondary brain injury, including neurological deficits, cerebral edema, and neuronal apoptosis. Moreover, VPA treatment upregulated the occurrence of autophagy and Nrf2/ARE pathway activity after TBI, and there was an increase in H3, H4 histone acetylation levels, accompanied by decreased transcriptional activity of the HDAC3 promoter in cortical lesions. These results suggest that VPA-mediated up-regulation of autophagy and antioxidative responses are likely due to increased activation of Nrf2/ARE pathway, through direct inhibition of HDAC3. This inhibition further reduces TBI-induced microglial activation and the subsequent inflammatory response, ultimately leading to neuroprotection.
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