Edaravone dexborneol provides neuroprotective benefits by suppressing ferroptosis in experimental intracerebral hemorrhage

作者：Han Li, Xiang Li, Mingzhi Li, Wenxin Li, Jinghui Wei, Yuming Huang, Haiqing Yan, Juntang Lin, Ping Zhang · 发表于：Scientific Reports · 年份：2025 · DOI：10.1038/s41598-025-99187-2 · 被引用次数：3 · 研究领域：Intracerebral and Subarachnoid Hemorrhage Research、Ferroptosis and cancer prognosis、Kruppel-like factors research

Edaravone dexborneol (EDB) is widely recognized for its anti-inflammatory and antioxidant properties and is clinically applied in the treatment of acute cerebral infarction. Ferroptosis is a critical process in the pathophysiology of brain injury following intracerebral hemorrhage (ICH). However, it remains unclear whether EDB can ameliorate ICH through the modulation of ferroptosis. This study aimed to evaluate the function and mechanism of EDB in treatment of ICH. With a male rat ICH model, animal behavior tests, histopathological staining, magnetic resonance imaging and evans blue staining were used to evaluate the neural protective function of EDB on ICH rats. The potential molecular mechanism was investigated using RNA sequencing. With the administration of Fer-1, a range of ferroptosis-related biomarkers, including Fe 2+ , 4-hydroxynonenal, malondialdehyde, etc., were analyzed to ascertain whether EDB confers neuroprotective effects through the modulation of P53/GPX4 pathways to inhibit ferroptosis. Finally, the findings were further corroborated using an in vitro ICH model with a P53 inhibitor. EDB has the potential to markedly enhance nerve and motor function, mitigate pathological damage, facilitate hematoma clearance, and repair BBB injury in ICH rats. KEGG analysis revealed that the differentially expressed genes were associated with signaling pathways, including P53 and ferroptosis. Both EDB and Fer-1 substantially reduced the concentrations of Fe 2+ , 4-hydroxyno...