ArticleHuman cell2025
Eucommia ulmoides (Duzhong) extract alleviates cerebral stroke by inhibiting ferroptosis-related gene DNA Damage-Inducible Transcript 4 (DDIT4) expression.
Article in Human cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- Ischemic Stroke and Traumatic Brain Injury: Epidemiology, Molecular Pathways, and Emerging Therapies.MedComm · 2026Review
- DDIT4 silencing attenuates sevoflurane-induced ferroptosis via the mTOR pathway in neuronal cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Ferroptosis in Ischemic Stroke: Insights from Natural Product Treatment and Future Directions.Drug design, development and therapy · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Cerebral stroke is an acute cerebrovascular disease, which is characterized by significant morbidity, death, and disability rate. Ischemic stroke is more than hemorrhagic stroke and accounts for 60-70% of all strokes. The present study explored the mechanisms of Eucommia ulmoides extract (EUE) in the treatment of ischemic stroke. Middle cerebral artery occlusion (MCAO) mouse models and oxygen and glucose deprivation (OGD) SH-SY5Y cell models were constructed to mimic ischemic stroke, and mice and cells were treated with gradient concentrations of EUE. The neurological function and brain tissue damage in mice were assessed using multiple parameters. Then the iron contents in cerebral tissue samples and neuronal cells were examined, and the expression levels of reactive oxygen species-related indicators and iron metabolism-related proteins were detected. EUE alleviated the ferroptosis process within cerebral tissue samples of MCAO mice and OGD-triggered neuronal cells, thereby mitigating neurological function and brain tissue damage by activating PI3K/Akt pathway. The target drug genes of EUE were searched by network pharmacology and molecular docking and found that the ferroptosis-related gene DDIT4 is the potential EUE-targeted gene in the therapy of ischemic stroke. DDIT4 expression was upregulated within cerebral brain samples of MCAO mice and OGD-triggered neuronal cells, and EUE could inhibit DDIT4 expression. The protective effect of EUE on neuronal cells could be partially reversed by overexpression of DDIT4. Moreover, EUE alleviated ferroptosis and improved neurological function in MCAO mice by suppressing DDIT4 expression and modulating the PI3K/Akt pathway. In conclusion, EUE exerts its neuroprotective effect against cerebral stroke by inhibiting DDIT4 expression and ferroptosis by regulating the PI3K/Akt pathway, and DDIT4 has been predicted to be an underlying therapeutic target for the treatment of ischemic stroke.
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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.