<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yuan B</submitter><funding>Natural Science Foundation</funding><pagination>9069825</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9288286</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>2022</volume><pubmed_abstract>Ferroptosis is a regulated cell death that characterizes the lethal lipid peroxidation and iron overload, which may contribute to early brain injury (EBI) pathogenesis after subarachnoid hemorrhage (SAH). Although Sirtuin 1 (SIRT1), a class III histone deacetylase, has been proved to have endogenous neuroprotective effects on the EBI following SAH, the role of SIRT1 in ferroptosis has not been studied. Hence, we designed the current study to determine the role of ferroptosis in the EBI and explore the correlation between SIRT1 and ferroptosis after SAH. The pathways of ferroptosis were examined after experimental SAH &lt;i>in vivo&lt;/i> (prechiasmatic cistern injection mouse model) and in HT-22 cells stimulated by oxyhemoglobin (oxyHb) &lt;i>in vitro&lt;/i>. Then, ferrostatin-1 (Fer-1) was used furth</pubmed_abstract><journal>Oxidative medicine and cellular longevity</journal><pubmed_title>Activation of SIRT1 Alleviates Ferroptosis in the Early Brain Injury after Subarachnoid Hemorrhage.</pubmed_title><pmcid>PMC9288286</pmcid><funding_grant_id>82071381</funding_grant_id><funding_grant_id>82072791</funding_grant_id><pubmed_authors>Zhou LJ</pubmed_authors><pubmed_authors>Zhao XD</pubmed_authors><pubmed_authors>Shen JD</pubmed_authors><pubmed_authors>Chen SJ</pubmed_authors><pubmed_authors>Huang HY</pubmed_authors><pubmed_authors>Yuan B</pubmed_authors><pubmed_authors>Wu Q</pubmed_authors><pubmed_authors>Han YL</pubmed_authors><pubmed_authors>Zhou XM</pubmed_authors><pubmed_authors>Lu XJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Activation of SIRT1 Alleviates Ferroptosis in the Early Brain Injury after Subarachnoid Hemorrhage.</name><description>Ferroptosis is a regulated cell death that characterizes the lethal lipid peroxidation and iron overload, which may contribute to early brain injury (EBI) pathogenesis after subarachnoid hemorrhage (SAH). Although Sirtuin 1 (SIRT1), a class III histone deacetylase, has been proved to have endogenous neuroprotective effects on the EBI following SAH, the role of SIRT1 in ferroptosis has not been studied. Hence, we designed the current study to determine the role of ferroptosis in the EBI and explore the correlation between SIRT1 and ferroptosis after SAH. The pathways of ferroptosis were examined after experimental SAH &lt;i>in vivo&lt;/i> (prechiasmatic cistern injection mouse model) and in HT-22 cells stimulated by oxyhemoglobin (oxyHb) &lt;i>in vitro&lt;/i>. Then, ferrostatin-1 (Fer-1) was used furth</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-29T10:40:06.428Z</modification><creation>2025-04-06T19:36:35.391Z</creation></dates><accession>S-EPMC9288286</accession><cross_references><pubmed>35855863</pubmed><doi>10.1155/2022/9069825</doi></cross_references></HashMap>