ArticleCNS neuroscience & therapeutics2024
Annexin A1 Mitigates Blood-Brain Barrier Disruption in a Sepsis-Associated Encephalopathy Model by Enhancing the Expression of Occludin and Zonula Occludens-1 (ZO-1).
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Article
- Hippocampal cytopathology orchestrates post-septic cognitive dysfunction.Metabolic brain disease · 2026Review
- Encephalopathy: Cause, Pathogenesis, and Treatment.MedComm · 2026Review
- Doxorubicin compromises blood-brain barrier integrity by suppressing annexin A1 expression.Open life sciences · 2026Article
- Review
- Extracellular vesicle signatures from eye lavage as novel non-invasive biomarkers for hypoxic ischaemic insult-findings from a neonatal mouse model.Frontiers in medical technology · 2025Article
- Emerging roles for interleukin-11 in the inflammatory response of intracerebral hemorrhage.Frontiers in neurology · 2025Review
- Gut-Brain Axis-Based Polygala Tenuifolia and Magnolia Officinalis Improve D-gal-Induced Cognitive Impairment in Mice Through cAMP and NF-κB Signaling Pathways.Drug design, development and therapy · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
aimsThis study investigated the protective role of Annexin A1 (ANXA1) in sepsis-associated encephalopathy (SAE) by examining its effects on brain vascular endothelium and blood-brain barrier (BBB) integrity.
methodsMice were divided into four groups: wild type (WT), cecal ligation and puncture (CLP), ANXA1 knockout (ANXA1[-/-]), and ANXA1(-/-) with CLP. Neurobehavioral changes were assessed using the Y-maze test, while BBB integrity was evaluated through Evans blue dye (EBD) staining and permeability tests with fluorescein isothiocyanate (FITC)-dextran.
resultsResults showed that ANXA1 levels were reduced in septic mice, and its deficiency exacerbated cognitive impairment and survival rate reduction. ANXA1 deficiency also upregulated proinflammatory cytokines and adhesion molecules, worsened BBB impairment, and altered expression of tight junction proteins and VEGF-A/VEGF-R2. In vitro, ANXA1 Ac2-26 prevented LPS-induced increased permeability in bEnd.3 cells by restoring tight junction proteins and reducing VEGF-A/VEGF-R2 expression. Notably, VEGF-A negated the protective effects of ANXA1 Ac2-26.
conclusionThe study concludes that ANXA1 reduces BBB permeability to protect against sepsis-induced brain dysfunction via VEGF-A/VEGF-R2 regulation of tight junction proteins, suggesting ANXA1 as a potential therapeutic for SAE.
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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 Socratic graph.