ArticleFrontiers in pharmacology2024
Naoqing formula alleviates acute ischaemic stroke-induced ferroptosis via activating
Article in Frontiers in pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Sinensetin attenuates post-stroke depression via dual modulation of TLR4/NF-κB-NRF2/GPX4 pathways.Scientific reports · 2026Article
- Ferroptosis in Ischemic Stroke: Insights from Natural Product Treatment and Future Directions.Drug design, development and therapy · 2026Review
- Integrated Transcriptomic and Proteomic Analysis Elucidates the Mechanisms of Huperzine A Injection Against Cerebral Ischemia/Reperfusion Injury.Drug design, development and therapy · 2026Article
- Gastrodin improves learning and memory in sleep-deprived mice through suppression of ferroptosis in hippocampal neurons via Nrf2.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The unmet promise: a critical review of antioxidant strategies in myocardial ischemia-reperfusion injury and the path towards precision medicine.Frontiers in pharmacology · 2025Review
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Authors and funding
12 authors.
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Abstract
Backgrounds: Ferroptosis is a form of regulated cell death. The accumulation of iron in the brain is linked to trigger ferroptosis after an ischaemic stroke (IS). Naoqing formula (NQ) is a traditional Chinese medicine metabolites with the clinical function of activating blood circulation, which is applied to treat IS clinically in China. Methods: Mice and SH-SY5Y cells were utilized to investigate the protective effects and the underlying mechanism of NQ against middle cerebral artery occlusion (MCAO) induced acute ischaemic stroke (AIS) and neuronal cellular ferroptosis caused by ferroptosis inducer Erastin Results: NQ attenuated AIS-induced neuronal damage and cerebral infarction by increasing cortical blood flow (CBF). Transcriptomics and proteomics analyses revealed that NQ might regulate lipid and iron metabolism through Conclusion: This study demonstrated that NQ protected against AIS via suppression of ferroptosis and oxidative stress, which were largely dependent on the upregulation of
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