<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chen Y</submitter><funding>Shenzhen Science and Technology Innovation Program</funding><funding>Shenzhen Key Medical Discipline Construction Fund</funding><pagination>e70495</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12368432</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>31(8)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>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.&lt;h4>Methods&lt;/h4>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 f</pubmed_abstract><journal>CNS neuroscience &amp; therapeutics</journal><pubmed_title>Oseltamivir Phosphate Modulates CD24-Siglec-G/10 Interaction to Suppress Microglial-Driven Neuroinflammation After Cardiac Arrest.</pubmed_title><pmcid>PMC12368432</pmcid><funding_grant_id>JCYJ20230807112007014</funding_grant_id><funding_grant_id>SZXK046</funding_grant_id><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Tang Z</pubmed_authors><pubmed_authors>Gong P</pubmed_authors><pubmed_authors>Li P</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Yu D</pubmed_authors><pubmed_authors>Sun Z</pubmed_authors><pubmed_authors>Li N</pubmed_authors><pubmed_authors>Wang L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Oseltamivir Phosphate Modulates CD24-Siglec-G/10 Interaction to Suppress Microglial-Driven Neuroinflammation After Cardiac Arrest.</name><description>&lt;h4>Background&lt;/h4>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.&lt;h4>Methods&lt;/h4>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 f</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Aug</publication><modification>2026-07-15T06:21:57.08Z</modification><creation>2026-06-30T03:23:41.811Z</creation></dates><accession>S-EPMC12368432</accession><cross_references><pubmed>40836885</pubmed><doi>10.1111/cns.70495</doi></cross_references></HashMap>