ArticleJournal of inflammation research2025
Perampanel Regulates Neuroinflammation and Ferroptosis via Activating FSP1 Following Brain Ischemia.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Anti-Inflammatory and Antioxidant Strategies in Epilepsy: From Molecular Mechanisms to Threshold Management.International journal of molecular sciences · 2026Review
- Celastrol Mitigates Acute Pancreatitis Associated Inflammation by Modulating the IL-34/CSF-1R Axis and Suppressing NF-κB/ERK Signaling.Journal of inflammation research · 2026Article
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Authors and funding
7 authors.
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Abstract
Purpose: Ischemic stroke remains a leading cause of global disability and mortality, with neuroinflammation and ferroptosis emerging as critical contributors to secondary neuronal damage. Perampanel, a non-competitive α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist, exhibits neuroprotective properties in neurological disorders, yet its mechanisms in ischemic stroke remain incompletely understood. This study investigated the therapeutic potential of post-injury perampanel administration in both in vivo and in vitro models, focusing on neuroinflammation, ferroptosis, and the role of ferroptosis suppressor protein 1 (FSP1). Methods: Rats received intraperitoneal perampanel (1.5 mg/kg) 10-15 minutes post-reperfusion for 3 days and exposed to middle cerebral artery occlusion (MCAO) for 60 minutes. Neurological function, neuronal survival, and markers of neuroinflammation and ferroptosis were assessed via immunostaining, Western blot, and behavioral tests. The in vitro ischemia model was mimicked by oxygen glucose deprivation (OGD) in primary cultured cortical neurons. Results: Perampanel significantly attenuated MCAO-induced neuronal loss (NeuN Conclusion: These findings demonstrate that perampanel mitigates post-ischemic brain injury by inhibiting neuroinflammation and neuronal ferroptosis via FSP1 activation. This study highlights FSP1 as a novel therapeutic target and positions perampanel as a promising candidate for ischemic stroke treatment, leveraging its established safety profile and clinical availability.
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