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Oxygen-glucose deprivation\/reperfusion (OGD\/R) model in vitro and the middle cerebral artery occlusion (MCAO) model in vivo were established to simulate cerebral I\/R injury. Sevoflurane postconditioning reduced neurological deficits, cerebral infarction, and ferroptosis after I\/R injury. Interestingly, sevoflurane significantly inhibited specificity protein 1 (SP1) expression in MACO rats and HT22 cells exposed to OGD\/R. SP1 overexpression attenuated the neuroprotective effects of sevoflurane on OGD\/R-treated HT22 cells, evidenced by reduced cell viability, increased apoptosis, and cleaved caspase-3 expression. Furthermore, chromatin immunoprecipitation and luciferase experiments verified that SP1 bound directly to the ACSL4 promoter region to increase its expression. In addition, sevoflurane inhibited ferroptosis via SP1\/ACSL4 axis. Generally, our study describes an anti-ferroptosis effect of sevoflurane against cerebral I\/R injury via downregulating the SP1\/ASCL4 axis. These findings suggest a novel sight for cerebral protection against cerebral I\/R injury and indicate a potential therapeutic approach for a variety of cerebral diseases.<\/jats:p>","DOI":"10.1177\/09603271231160477","type":"journal-article","created":{"date-parts":[[2023,2,26]],"date-time":"2023-02-26T21:03:04Z","timestamp":1677445384000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":34,"title":["Sevoflurane Postconditioning Attenuates Cerebral Ischemia-Reperfusion Injury by Inhibiting SP1\/ACSL4-Mediated Ferroptosis"],"prefix":"10.1177","volume":"42","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1674-8411","authenticated-orcid":false,"given":"Ning","family":"Lyu","sequence":"first","affiliation":[{"name":"Department of Anesthesiology, Tianjin Central Hospital of Gynecology Obstetrics, Tianjin, 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