ArticleMetabolic brain disease2025
Luteolin ameliorates ischemic/reperfusion injury by inhibiting ferroptosis.
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 8 papers.
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Who cites it
8 citing papers in PubMed.
- Luteolin Attenuates Hypoxia-Induced Ferroptosis in Human Brain Microvascular Endothelial Cells Through Modulation of the PPARγ/FABP5/ALOX15 Signaling Pathway.Biomedicines · 2026Article
- Luteolin in osteoarticular diseases: a review of preclinical studies and translational perspectives.Inflammopharmacology · 2026Review
- Traditional Chinese Medicine Targeting Ferroptosis in Cardiovascular Diseases: Advances and Perspectives.Journal of cardiovascular translational research · 2026Review
- Ferroptotic neurodegeneration and diet: a narrative review.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Luteolin and neuroinflammation: a multi-target therapeutic strategy for central nervous system disorders.Frontiers in pharmacology · 2026Review
- Ferroptosis in Ischemic Stroke: Insights from Natural Product Treatment and Future Directions.Drug design, development and therapy · 2026Review
- Review
- Luteolin Potentially Alleviates Methamphetamine Withdrawal-Induced Negative Emotions and Cognitive Deficits Through the AKT/FOXO1/HO-1 Signaling Pathway in the Prefrontal Cortex and Caudate Putamen.International journal of molecular sciences · 2025Article
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9 authors.
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Abstract
Ischaemic stroke is a large disease burden worldwide. Thrombolysis and thrombectomy are the main treatment methods for cerebral ischemia-reperfusion (I/R) injury. Luteolin, as a flavonoid compound, has an antagonistic effect on inflammation, oxidative stress, and tumorigenesis in disease. Therefore, the primary objective of this study is to determine the role of luteolin in cerebral I/R injury. Oxygen glucose deprivation/reoxygenation (OGD/R)-treated BV2 cells and a cerebral I/R rat model were established. Cell viability and death were verified using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and propidium iodide staining. The glutathione/oxidized glutathione (GSH/GSSG) ratio, superoxide dismutase (SOD) activity, and reactive oxygen species (ROS) and malondialdehyde (MDA) levels were determined using corresponding kits. Solute Carrier Family 7 Member 11 (SLC7A11), nuclear transcription factor erythroid 2-related factor 2 (NRF2), and glutathione peroxidase 4 (GPX4) levels were analyzed by western blotting. In addition, the infarct volume of brain tissues was examined by tetrazolium chloride (TTC) staining. Luteolin treatment significantly enhanced cell viability, decreased LDH release and intracellular ROS and MDA levels, and increased the GSH/GSSG ratio and SOD activity in OGD/R-treated BV2 cells. PI staining demonstrated that cell death was inhibited after luteolin treatment. Additionally, luteolin treatment significantly increased the SLC7A11, NRF2, and GPX4 protein levels. After treatment with ML385, an NRF2 inhibitor, the influence of luteolin on OGD/R-treated BV2 cells was reversed. Moreover, luteolin treatment significantly decreased the neurological score and infarct area in the brain tissues of cerebral I/R rats. Our research demonstrated that luteolin treatment inhibited ferroptosis by enhancing antioxidant functions through the NRF2 pathway, which provides a promising method for treating cerebral I/R injury.
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