ArticleMetabolic brain disease2025
Edaravone dextranol alleviates ferroptosis, Cuproptosis, and blood-brain barrier damage after acute cerebral infarction.
Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Cuproptosis in Ischemic Stroke: Molecular Mechanisms and Therapeutic Potential.Molecules (Basel, Switzerland) · 2026Review
- Advances in ferroptosis and cuproptosis: implications for spinal cord injury.Molecular biology reports · 2026Review
- Cuproptosis: Biomarkers, Mechanisms and Treatments in Diseases.Molecules (Basel, Switzerland) · 2026Review
- Biomimetic M2 microglia membrane-coated nanoplatform for immune reprogramming and targeted edaravone delivery in ischemic stroke.Regenerative biomaterials · 2026Article
- Key copper homeostasis genes and inflammatory mechanisms in ischemic stroke: A bioinformatics and experimental study.Functional & integrative genomics · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Edaravone dextrose (EDB) is a commonly used clinical treatment for cerebral infarction due to its anti-inflammatory and free radical scavenging properties. However, its potential additional neuroprotective mechanisms need to be further investigated. In this study, we evaluated the effects of EDB on ferroptosis, cuproptosis, and blood-brain barrier (BBB) disruption after cerebral infarction in vivo and in vitro by constructing a mouse middle cerebral artery occlusion (MCAO) model, and an oxygen-glucose deprivation/reperfusion (OGD/R) model of neurons and brain microvascular endothelium. Our results showed that EDB treatment improved neurological impairment and brain histopathology in MCAO mice. EDB treatment significantly alleviated ferroptosis and cuproptosis in MCAO mice and OGD/R models of neuronal, in vitro and in vivo, the protective pathway of ferroptosis SLC7A11/GPX4 was detected to be activated and the cuproptosis-promoting protein SLC31A1 and FDX1 were down-regulated. We also found that EDB treatment ameliorated BBB damage in MCAO mice. The endothelial cell protective pathway PDGFRβ/PI3K/AKT activation was also detected in MCAO mice and OGD/R models of endothelial cells after EDB treatment. In conclusion, our study demonstrated that EDB has a good ameliorating effect on ferroptosis, cuproptosis, and BBB damage after cerebral infarction, which provides more evidence for the clinical application of EDB and provides new theories and directions for the study of the mechanism of EDB.
Indexed as
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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.