ArticleFrontiers in pharmacology2025
Neuroprotective effects of ethanol extraction from
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Neuromodulation Techniques in Chronic Cerebral Hypoperfusion: Mechanisms and Therapeutic Advances.CNS neuroscience & therapeutics · 2026Review
- Protective Effect ofCurrent issues in molecular biology · 2026Article
- Inhibition of RBM23 induces ferroptosis in colon cancer cells via c-Myc regulation.Cancer cell international · 2026Article
- Ferroptosis and the eye: bridging the gap between cell death and vision preservation.Frontiers in immunology · 2026Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Vascular dementia (VD) is a neurodegenerative disease caused by chronic cerebral hypoperfusion (CCH), which considerably impact patients' quality of life. Ethanol extraction from Methods: After 30 days of RY-A gavage treatment in a CCH rat model, its effects were evaluated using the Morris water maze test, cerebral blood flow measurements, and HE staining of the brain. These findings, combined with serum medicinal chemistry, RNA-seq, and metabolomics analyses, revealed the active compounds and mechanisms of RY-A in CCH rats. The results were further validated using assay kits and Western blot techniques. Results: RY-A treatment significantly attenuated neurological damage and improved cognitive function in CCH rats. Ultra-high-performance liquid chromatography high-resolution mass spectrometry identified 511 blood-entry compounds of RY-A. RNA-seq and metabolomic analysis showed that RY-A might help to normalize changes in gene and metabolite expression caused by CCH. RY-A induced neuroprotective effects by increasing the production of key proteins involved in ferroptosis inhibition, such as SLC7A11, SLC3A2, GSS, and GPX4, while increasing antioxidant enzyme activities and alleviating oxidative stress. Conclusion: RY-A inhibited oxidative stress and ferroptosis by activating the System Xc-/GSH/GPX4 pathway and balancing iron metabolism, thereby attenuating CCH-induced neurological damage and cognitive deficits.
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Registered trials
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