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Article Abstract
Purpose: Ischemia-reperfusion injury remains a major problem following myocardial infarction. Alpinetin (ALPT) has been reported to exhibit cardioprotective effects as well as resistance to ischemia-reperfusion injury. However, its role and mechanism during myocardial ischemia-reperfusion injury are unknown.
Methods: The anoxia/reoxygenation (A/R) injury model of H9c2 cells and the ischemia reperfusion(I/R) injury model of Sprague-Dawley rats were used in this study. Multiple indicator evaluations, flow cytometry, western blot, and transmission electron microscopy were performed to assess the protective effect of alpinetin pretreatment and its mechanism of action. In addition, the role of mitochondrial ferritin (FTMT) in alpinetin-based protection was investigated using pAD/FTMT-shRNA. The experimental findings were ultimately validated in rat I/R injury models.
Results: Similar to ferrostatin-1, alpinetin decreased prostaglandin-endoperoxide synthase 2 (PTGS2), lactate dehydrogenase, malondialdehyde, ferrous iron, reactive oxygen species, and oxidized glutathione disulfide (GSSG) levels and increased cell viability, glutathione (GSH) levels, the GSH/GSSG ratio, and glutathione peroxidase 4 protein levels in the injury models. Alpinetin also reversed A/R injury-induced increased caspase-3 activity and apoptosis rate and decreased Bcl-2/Bax ratio and mitochondrial membrane potential level. Of note, alpinetin attenuated mitochondrial damage induced by A/R injury. These protective effects were blocked via FTMT silencing.
Conclusion: Alpinetin protects against myocardial ischemia-reperfusion injury by inhibiting ferroptosis and apoptosis via FTMT.
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| http://dx.doi.org/10.1016/j.ejphar.2025.178123 | DOI Listing |
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