ArticleMolecular biology reports2025
Edaravone reduces brain injury in hepatic encephalopathy by upregulation of Nrf2/HO-1 and inhibition of NF-κB, iNOS/NO and inflammatory cytokines.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The role of systemic inflammation in hepatic encephalopathy: advances in inflammatory mechanisms, prevention and treatment research.Annals of medicine · 2026Review
- Protective Effect of Edaravone on Doxorubicin-Induced Thyroid Dysfunction in Rats Revealed byMedicina (Kaunas, Lithuania) · 2026Article
- Trigonelline protects against alcohol-induced brain damage by inhibition of oxidative stress, TLR4/NF-κB/proinflammatory cytokines pathway, and apoptosis.Iranian journal of basic medical sciences · 2026Article
- Machine learning-based transcriptomic analysis identifies candidate genes in sepsis-induced coagulopathy and explores the immunomodulatory potential of baicalein.Human genomics · 2025Article
- Matrix metalloproteinase‑9 in hemorrhagic transformation after acute ischemic stroke (Review).Molecular medicine reports · 2025Review
- The Role of Neuroinflammation in the Pathogenesis of Hepatic Encephalopathy.Journal of immunology research · 2025Review
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Authors and funding
2 authors.
Funding
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Abstract
backgroundBrain damage is the most important complication in patients with hepatic encephalopathy (HE). Oxidative stress and inflammation are essential factors in the progression of brain injury caused by HE. The aim of this study was to investigate the potential therapeutic effect of edaravone and its underlying mechanisms against brain injury associated with HE in mice. METHODS AND
resultsHE was induced by the injection of thioacetamide (200 mg/kg) for 2 days and then mice treated with edaravone (10 or 20 mg/kg/day, ip) for four consecutive days. The brain tissues were dissected for histopathological, biochemical, ELISA, RT-qPCR and immunofluorescence analysis. The results showed that edaravone improved the locomotor function and ameliorated brain histopathological changes in mice with HE. Edaravone inhibited oxidative stress markers by increasing the levels of glutathione, catalase, superoxide dismutase, glutathione reductase and the upregulation of nuclear erythroid 2-related factor (Nrf2)/HO-1 pathway in the brain tissue. Administration of edaravone significantly decreased the expression of p-NF-κB and iNOS. Edaravone treatment reduced the levels of NO, MPO and MMP-9 in the brain of mice. Additionally, the brain levels and expressions of inflammatory cytokines IL-1β, IL-6, TNF-α and IFN-γ were downregulated in mice treated with edaravone.
conclusionsThese results suggest that edaravone exerts significant neuroprotection by modulating of inflammatory and oxidative responses in HE and may serve as a promising agent for the treatment of brain injury associated with HE.
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