ArticleImmunity, inflammation and disease2023
Hyperglycemia disrupted the integrity of the blood-brain barrier following diffuse axonal injury through the sEH/NF-κB pathway.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Atherogenic Index of Plasma for the Prediction of Delirium in ICU Patients: A Retrospective Cohort Study Based on the MIMIC-IV Database.Brain and behavior · 2026Article
- Inhibition of IL-17 Alleviates Blood-Brain Barrier Disruption Following Diffuse Axonal Injury Accompanied by Hyperglycemia Through the NF-κB Pathway.Mediators of inflammation · 2026Article
- Triglyceride-Glucose Index and Short-Term Functional Prognosis in Patients With Acute Ischemic Stroke: A Retrospective Study.Brain and behavior · 2025Article
- Short-Term: Cellular Metabolism and Gene Expression During the Onset of Diabetic Kidney Disease: A Diabetes Mellitus Experimental Model.International journal of molecular sciences · 2025Article
- Relationship between blood-cerebrospinal fluid barrier integrity, cardiometabolic, and inflammatory factors in schizophrenia-spectrum disorders.Brain, behavior, & immunity - health · 2025Article
- Risk Factors and Outcomes of Hemorrhagic Transformation in Acute Ischemic Stroke Following Thrombolysis: Analysis of a Single-Center Experience and Review of the Literature.Medicina (Kaunas, Lithuania) · 2025Review
- Metabolic disorders after traumatic brain injury: a narrative review of systemic consequences.Metabolic brain disease · 2025Review
- Hyperglycemia disrupted the integrity of the blood-brain barrier following diffuse axonal injury through the sEH/NF-κB pathway.Immunity, inflammation and disease · 2023Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
objectivesWe aimed to investigate the role of soluble epoxide hydrolase for hyperglycemia induced-disruption of blood-brain barrier (BBB) integrity after diffuse axonal injury (DAI).
methodsRat DAI hyperglycemia model was established by a lateral head rotation device and intraperitoneal injection of 50% glucose. Glial fibrillary acidic protein, ionized calcium-binding adapter molecule-1, β-amyloid precursor protein, neurofilament light chain, and neurofilament heavy chain was detected by immunohistochemistry. Cell apoptosis was examined by terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) assay. The permeability of blood-brain barrier (BBB) was assessed by expression of tight junction proteins, leakage of Evans blue and brain water content. The soluble epoxide hydrolase (sEH) pathway was inhibited by 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea (TPPU) and the nuclear transcription factor kappa B (NF-κB) pathway was inhibited by pyrrolidine dithiocarbamate and activated by phorbol-12-myristate-13-acetate in vivo and/or vitro, respectively. The inflammatory factors were detected by enzyme-linked immunosorbent assay.
resultsHyperglycemia could exacerbate axonal injury, aggravate cell apoptosis and glial activation, worsen the loss of BBB integrity, increase the release of inflammatory factors, and upregulate the expression of sEH and NF-κB. Inhibition of sEH could reverse all these damages and protect BBB integrity by upregulating the expression of tight junction proteins and downregulating the levels of inflammatory factors in vivo and vitro, while the agonist of NF-κB pathway abrogated the protective effects of TPPU on BBB integrity in vitro.
conclusionssEH was involved in mediating axonal injury induced by hyperglycemia after DAI by disrupting BBB integrity through inducing inflammation via the NF-κB pathway.
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