ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
Eupatilin mitigates ICH-induced brain injury via SOX2/SLC7A11 regulation of ferroptosis.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
The trial behind it
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
2 citing papers in PubMed.
- Combined Dihydroartemisinin and Eupatilin Suppress Prostate Cancer through AR-Associated Ferroptosis and Modulation of Macrophage-Tumor Crosstalk.Research (Washington, D.C.) · 2026Article
- Traditional Chinese Medicine and Ferroptosis in Intracerebral Hemorrhage: A Potential Therapeutic Approach.Drug design, development and therapy · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Intracerebral hemorrhage (ICH) is an acute and potentially fatal brain disease that causes severe brain damage, resulting in hemiplegia, speech disorders, and even coma or death. Recently, oxidative stress and ferroptosis are claimed involved in the pathogenesis of ICH brain injury. Eupatilin (EUP) is a flavonoid component with promising anti-inflammatory and anti-oxidative stress properties. The present study aimed to explore the pharmacological activity and potential mechanisms of EUP in treating ICH brain injury from the respect of ferroptosis. The ICH model was established in mouse, followed by treating with 3 and 10 mg/kg EUP. Elevated mNSS score, increased brain water content, reduced Nissl bodies, and enhanced EB concentrations were observed in ICH mice, which were sharply alleviated by EUP treatments. Furthermore, increased ROS, MDA, and iNOS levels; declined SOD activities; and enhanced proinflammatory factors like interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and interleukin-1β (IL-1β) in ICH mice were remarkably reversed by EUP. In addition, increased iron
Indexed as
Identifiers
40047856What Socratic holds
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.