ArticleJournal of neurochemistry2012
Attenuation of neonatal ischemic brain damage using a 20-HETE synthesis inhibitor.
Article in Journal of neurochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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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
35 citing papers in PubMed, 43 citations in OpenAlex.
- Sex-dependent role of 20-HETE synthesis in outcome from ischemic stroke in rats.Physiological reports · 2026Article
- Neuroprotection provided by hypothermia initiated with high transnasal flow with ambient air in a model of pediatric cardiac arrest.American journal of physiology. Regulatory, integrative and comparative physiology · 2024Article
- Calpain as a Therapeutic Target for Hypoxic-Ischemic Encephalopathy.Molecular neurobiology · 2024Review
- Identification of Metabolomic Signatures for Ischemic Hypoxic Encephalopathy Using a Neonatal Rat Model.Children (Basel, Switzerland) · 2023Article
- Candidate neuroinflammatory markers of cerebral autoregulation dysfunction in human acute brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Review
- Reactive oxygen species-responsive HET0016 prodrug-loaded liposomes attenuate neuroinflammation and improve neurological deficit in a rat model of juvenile traumatic brain injury.Frontiers in neuroscience · 2023Article
- Cytochrome P450-derived eicosanoids in brain: From basic discovery to clinical translation.Advances in pharmacology (San Diego, Calif.) · 2023Article
- Long-term cold storage preservation does not affect fatty livers from rats fed with a methionine and choline deficient diet.Lipids in health and disease · 2021Article
- 20-HETE synthesis inhibition attenuates traumatic brain injury-induced mitochondrial dysfunction and neuronal apoptosis via the SIRT1/PGC-1α pathway: A translational study.Cell proliferation · 2021Article
- 20-HETE Participates in Intracerebral Hemorrhage-Induced Acute Injury by Promoting Cell Ferroptosis.Frontiers in neurology · 2021Article
- Review
- Sulforaphane Protects Piglet Brains from Neonatal Hypoxic-Ischemic Injury.Developmental neuroscience · 2020Article
- The Role of Mitochondrial and Endoplasmic Reticulum Reactive Oxygen Species Production in Models of Perinatal Brain Injury.Antioxidants & redox signaling · 2019Article
- 20-HETE synthesis inhibition promotes cerebral protection after intracerebral hemorrhage without inhibiting angiogenesis.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
- Administration of a 20-Hydroxyeicosatetraenoic Acid Synthesis Inhibitor Improves Outcome in a Rat Model of Pediatric Traumatic Brain Injury.Developmental neuroscience · 2019Article
- Perinatal hypoxic-ischemic brain injury in large animal models: Relevance to human neonatal encephalopathy.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Review
- The contribution of TRPV1 channel to 20-HETE-Aggravated ischemic neuronal injury.Prostaglandins & other lipid mediators · 2018Review
- P450 Eicosanoids and Reactive Oxygen Species Interplay in Brain Injury and Neuroprotection.Antioxidants & redox signaling · 2018Article
- 20-HETE Inhibition by HET0016 Decreases the Blood-Brain Barrier Permeability and Brain Edema After Traumatic Brain Injury.Frontiers in aging neuroscience · 2018Article
- Liver Graft Susceptibility during Static Cold Storage and Dynamic Machine Perfusion: DCD versus Fatty Livers.International journal of molecular sciences · 2017Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
20-Hydroxyeicosatetraenoic acid (20-HETE) is a cytochrome P450 metabolite of arachidonic acid that that contributes to infarct size following focal cerebral ischemia. However, little is known about the role of 20-HETE in global cerebral ischemia or neonatal hypoxia-ischemia (H-I). The present study examined the effects of blockade of the synthesis of 20-HETE with N-hydroxy-N'-(4-n-butyl-2-methylphenyl) formamidine (HET0016) in neonatal piglets after H-I to determine if it protects highly vulnerable striatal neurons. Administration of HET0016 after H-I improved early neurological recovery and protected neurons in putamen after 4 days of recovery. HET0016 had no significant effect on cerebral blood flow. cytochrome P450 4A immunoreactivity was detected in putamen neurons, and direct infusion of 20-HETE in the putamen increased phosphorylation of Na(+), K(+) -ATPase and NMDA receptor NR1 subunit selectively at protein kinase C-sensitive sites but not at protein kinase A-sensitive sites. HET0016 selectively inhibited the H-I induced phosphorylation at these same sites at 3 h of recovery and improved Na(+), K(+) -ATPase activity. At 3 h, HET0016 also suppressed H-I induced extracellular signal-regulated kinase 1/2 activation and protein markers of nitrosative and oxidative stress. Thus, 20-HETE can exert direct effects on key proteins involved in neuronal excitotoxicity in vivo and contributes to neurodegeneration after global cerebral ischemia in immature brain.
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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.