ArticleFrontiers in pharmacology2025
Intracerebroventricular calycosin attenuates cerebral ischemia-reperfusion injury in rats via HMGB1-dependent pyroptosis inhibition.
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.
- Cell death in ischemia-reperfusion injury: beyond a single-cell-death perspective.Biomarker research · 2026Review
- Pyroptosis in cerebral ischemia‑reperfusion injury: Molecular mechanisms and therapeutic implications (Review).Molecular medicine reports · 2026Review
- Involvement of the pyroptosis-HMGB1 axis in systemic diseases.Frontiers in cell and developmental biology · 2026Review
- Protective Effect of Chinese Herbal Medicine on Cerebral Ischemia-Reperfusion Injury by Regulating Ferroptosis.Drug design, development and therapy · 2026Review
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Authors and funding
9 authors.
Funding
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Abstract
Introduction: HMGB1-NLRP3 mediated pyroptosis was recently discovered to be a pathogenic cause of ischemic stroke. Our previous research has demonstrated the anti-inflammatory and anti-apoptotic properties of calycosin in mitigating cerebral ischemia-reperfusion injury (CIRI). However, its specific effects on HMGB1-NLRP3-mediated pyroptosis in ischemic stroke remain unclear. This study investigated the efficacy of calycosin in reducing pyroptosis-linked CIRI. Methods: Results and Discussion: Calycosin significantly reduced neurological impairments and brain infarction in a dose-dependent manner, alleviated neuronal damage and decreased the expression of pyroptosis-related markers, including NLRP3, GSDMD, HMGB1, IL-1β, IL-18, and caspase-1. These results indicate that calycosin enhances microglial cell survival and mitigates pyroptotic damage by inhibiting NLRP3 inflammasome activation, suggesting its potential as a neuroprotective therapy for ischemic stroke through the modulation of the HMGB1-dependent pyroptosis pathway.
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Registered trials
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