ArticleFrontiers in aging neuroscience2018
20-HETE Inhibition by HET0016 Decreases the Blood-Brain Barrier Permeability and Brain Edema After Traumatic Brain Injury.
Article in Frontiers in aging neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed, 14 citations in OpenAlex.
- 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
- Vascular contributions to cognitive impairment and dementia: the emerging role of 20-HETE.Clinical science (London, England : 1979) · 2021Review
- Review
- The Impact of Gut Microbiota Disorders on the Blood-Brain Barrier.Infection and drug resistance · 2020Review
- 20-HETE Enzymes and Receptors in the Neurovascular Unit: Implications in Cerebrovascular Disease.Frontiers in neurology · 2020Article
- Resolvin D1 ameliorates Inflammation-Mediated Blood-Brain Barrier Disruption After Subarachnoid Hemorrhage in rats by Modulating A20 and NLRP3 Inflammasome.Frontiers in pharmacology · 2020Article
- Evaluating differential nanoparticle accumulation and retention kinetics in a mouse model of traumatic brain injury via KScientific reports · 2019Article
- Conflicting Roles of 20-HETE in Hypertension and Stroke.International journal of molecular sciences · 2019Review
- Diabetes inhibits corneal epithelial cell migration and tight junction formation in mice and human via increasing ROS and impairing Akt signaling.Acta pharmacologica Sinica · 2019Article
- Administration of a 20-Hydroxyeicosatetraenoic Acid Synthesis Inhibitor Improves Outcome in a Rat Model of Pediatric Traumatic Brain Injury.Developmental neuroscience · 2019Article
Corrections and comments
- Retraction · 2024-07-28Concerns/Issues about Data · Concerns/Issues about Image · Duplication of Data · Duplication of/in Image · Investigation by Journal/Publisher · Investigation by Third Party · Original Data and/or Images not Provided and/or not Available · Unreliable Data · Unreliable Results and/or Conclusions · Upgrade/Update of Prior Notice(s) · · See also: https://pubpeer.com/publications/4BFF79A3DDAFB40BD59A88E6A95F7D
- Correction · 2018-08-19Error in Text · Updated to Retraction · · See also: https://pubpeer.com/publications/4BFF79A3DDAFB40BD59A88E6A95F7D
- Erratum issued
- Retracted
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have implicated 20-HETE as a vasoconstrictive mediator in trauma, the purpose of this study was to determine whether administration of HET0016, the 20-HETE inhibitor, could protect neurons from trauma and the effect of HET0016 on the blood-brain barrier (BBB) and brain edema in experimental traumatic brain injury (TBI). Rat models with TBI were established. Brain edema was measured according to the wet and dry weight method at 3, 24, and 72 h after injury. The BBB permeability was quantified by dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI). Superoxide production, the activity of superoxide dismutase (SOD) and total antioxidative capability (T-AOC) in traumatic brain tissues were also measured. Western blot analysis was used to analyze the expression of the occludin, ZO-1, Matrix metalloproteinase-9 (MMP-9), and c-Jun N-terminal protein kinase (JNK) pathways. At 24 and 72 h after administration of HET0016 following TBI, the BBB permeability and brain edema decreased. The decrease in superoxide production and the increase in the activity of SOD and T-AOC were measured in this study. Western blot analysis showed that the expression of MMP-9 and JNK pathways was suppressed, but the expression of ZO-1 and occludin was increased. These results suggest that the administration of HET0016 could protect the BBB function and decrease brain edema after experimental traumatic injury by suppressing the expression of MMP-9 and activating the expression of tight junction proteins via suppressing the JNK pathway and oxidative stress.
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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.