ArticleJournal of molecular neuroscience : MN2016
Post-Injury Administration of Tert-butylhydroquinone Attenuates Acute Neurological Injury After Intracerebral Hemorrhage in Mice.
Article in Journal of molecular neuroscience : MN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 35 citations in OpenAlex.
- CORM-2 protects against sepsis-associated encephalopathy by activating the Nrf2/SLC7A11/GPX4 axis to inhibit ferroptosis and neuroinflammation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Neuroprotection From Intracerebral Hemorrhage Following Pharmacological Inhibition of GSK3β Depends on HFE Gene Status.Journal of neurochemistry · 2026Article
- Common Mutation in theStroke · 2023Article
- Dysregulation of Serum MicroRNA after Intracerebral Hemorrhage in Aged Mice.Biomedicines · 2023Article
- Review
- The Role of Concomitant Nrf2 Targeting and Stem Cell Therapy in Cerebrovascular Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Transcription factor nuclear factor erythroid 2 p45-related factor 2 (NRF2) ameliorates sepsis-associated acute kidney injury by maintaining mitochondrial homeostasis and improving the mitochondrial function.European journal of histochemistry : EJH · 2022Article
- Potential therapeutic effects of Nrf2 activators on intracranial hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Review
- Entinostat improves acute neurological outcomes and attenuates hematoma volume after Intracerebral Hemorrhage.Brain research · 2021Article
- Microglia Phenotype and Intracerebral Hemorrhage: A Balance of Yin and Yang.Frontiers in cellular neuroscience · 2021Article
- A Combined Proteomics and Bioinformatics Approach Reveals Novel Signaling Pathways and Molecular Targets After Intracerebral Hemorrhage.Journal of molecular neuroscience : MN · 2020Article
- miR-183-5p alleviates early injury after intracerebral hemorrhage by inhibiting heme oxygenase-1 expression.Aging · 2020Article
- NRF2 Regulation Processes as a Source of Potential Drug Targets against Neurodegenerative Diseases.Biomolecules · 2020Review
- Role of Nrf2 and Its Activators in Cardiocerebral Vascular Disease.Oxidative medicine and cellular longevity · 2020Review
- Differential Cellular Expression of Galectin-1 and Galectin-3 After Intracerebral Hemorrhage.Frontiers in cellular neuroscience · 2019Article
- A combination antioxidant therapy to inhibit NOX2 and activate Nrf2 decreases secondary brain damage and improves functional recovery after traumatic brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Article
- Tert-butylhydroquinone post-treatment attenuates neonatal hypoxic-ischemic brain damage in rats.Neurochemistry international · 2018Article
- [Frontiers in neuroscience · 2018Article
- Research Progress in Understanding the Relationship Between Heme Oxygenase-1 and Intracerebral Hemorrhage.Frontiers in neurology · 2018Review
- Microglia and CNS Interleukin-1: Beyond Immunological Concepts.Frontiers in neurology · 2018Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracerebral hemorrhage (ICH) is a severe form of stroke with substantial public health impact. Notably, there is no effective treatment for ICH. Given the role of transcription factor Nrf2 (NF-E2-related factor 2) in antioxidant signaling, herein, we tested the efficacy of tert-butylhydroquinone (TBHQ), a selective inducer of Nrf2 in a preclinical model of ICH. Male CD1 mice were subjected to experimental intracerebral hemorrhage and administered intraperitoneally with TBHQ. The administration of TBHQ enhanced the DNA-binding activity of Nrf2 in the brain and reduced oxidative brain damage in comparison to vehicle-treated ICH. In addition, TBHQ treatment reduced microglial activation with concomitant reduction in the release of proinflammatory cytokine interleukin-1β (IL-1 β). Furthermore, TBHQ treatment attenuated neurodegeneration and improved neurological outcomes after ICH. Altogether, the data demonstrate the efficacy of post-injury administration of TBHQ in attenuating acute neurological injury after ICH.
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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.