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Oseltamivir Phosphate Modulates CD24‐Siglec‐G/10 Interaction to Suppress Microglial‐Driven Neuroinflammation After Cardiac Arrest
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Oseltamivir Phosphate Modulates CD24‐Siglec‐G/10 Interaction to Suppress Microglial‐Driven Neuroinflammation After Cardiac Arrest
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Journal Article
Oseltamivir Phosphate Modulates CD24‐Siglec‐G/10 Interaction to Suppress Microglial‐Driven Neuroinflammation After Cardiac Arrest
2025
Overview
Background In cardiac arrest (CA) patients undergoing cardiopulmonary resuscitation (CPR), neuroinflammation following return of spontaneous circulation (ROSC) contributes to brain ischemia/reperfusion injury and neurological dysfunction. Recent evidence suggested that neuraminidase could exacerbate inflammatory responses by disrupting CD24‐Siglec‐G/10 immune checkpoint axis. As a neuraminidase inhibitor, oseltamivir phosphate (OP) holds potential for immunomodulation beyond its antiviral use. We aimed to investigate the impact and mechanism of OP on neuroinflammation regulation after ROSC. Methods Male pigs were randomized into the sham control group, CPR, and CPR + OP group. CA was induced in pigs through 8 min of untreated ventricular fibrillation. Brains were harvested for assessing serum inflammatory markers and neuronal damage at 24 h after ROSC. BV2 microglial underwent oxygen–glucose deprivation/reperfusion (OGD/R). Effects of OP on inflammatory responses, NF‐κB activation, cell viability, and the CD24‐Siglec‐G/10 interaction were evaluated using immunofluorescence, immunoprecipitation, molecular, and biochemical assays. Results In vivo, OP attenuated pig cerebral microglial activation and neuronal integrity with attenuated neuroinflammation, alongside time‐dependent neuraminidase activity increases. In vitro, OP suppressed OGD/R‐induced microglial NF‐κB activation, reduced pro‐inflammatory cytokine levels, and preserved CD24‐Siglec‐G interaction, correlating with diminished neuraminidase release. Conclusions OP as a repurposed immunomodulator that suppresses microglial‐driven neuroinflammation after CA by preserving sialylation‐dependent CD24‐Siglec‐G/10 interaction. The schematic diagram demonstrates how oseltamivir phosphate (OP, Tamiflu) alleviates cerebral injury and neuroinflammation after cardiac arrest/cardiopulmonary resuscitation (CA/CPR) through the CD24‐Siglec‐G/10 axis. The interaction between CD24 and Siglec‐G/10 via sialic acid restrains NF‐κB p65 nuclear translocation. This molecular inhibitory mechanism is compromised by neuraminidase during ischemia‐reperfusion injury, while OP exerts neuroprotection through targeted inhibition of desialylation, offering therapeutic opportunities.
Publisher
John Wiley & Sons, Inc,John Wiley and Sons Inc
Subject
/ Cardiopulmonary Resuscitation
/ CD24
/ Cerebrum
/ CPR
/ Glucose
/ Heart
/ Heart Arrest - complications
/ Ischemia
/ Male
/ Neuroinflammatory Diseases - drug therapy
/ Neuroinflammatory Diseases - etiology
/ Neuroinflammatory Diseases - metabolism
/ NF‐κB
/ Original
/ Oseltamivir - therapeutic use
/ Swine
