Fluoxetine attenuates hepatic ischemia–reperfusion injury through antioxidant, anti‑inflammatory and anti‑apoptotic mechanisms

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dc.authorid0000-0002-1116-337X
dc.authorid0000-0003-0557-1884
dc.authorid0000-0002-4737-3053
dc.authorid0000-0003-3561-3977
dc.authorid0000-0002-2513-6612
dc.authorid0000-0002-1926-6947
dc.contributor.authorIşık, Musab
dc.contributor.authorŞahin, Gülderen
dc.contributor.authorKervancıoğlu, Gülnaz
dc.contributor.authorGüner, İbrahim
dc.contributor.authorYaman, Muhittin Onur
dc.contributor.authorYelmen, Nermin
dc.date.accessioned2026-06-25T14:25:08Z
dc.date.available2026-06-25T14:25:08Z
dc.date.issued2026
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Histoloji ve Embriyoloji Ana Bilim Dalı
dc.description.abstractHepatic ischemia–reperfusion injury is a major clinical problem associated with liver surgery, trauma, and transplantation, characterized by oxidative stress, inflammation, microcirculatory dysfunction, and apoptosis. Fluoxetine, a selective sero tonin reuptake inhibitor, has been reported to exert antioxidant, anti-inflammatory, and antiapoptotic effects. The present study aimed to investigate the potential protective effects of fluoxetine against experimental hepatic ischemia–reperfusion injury in rats. Male Wistar rats were randomly assigned to three groups: control, ischemia–reperfusion and fluoxetine-treated ischemia–reperfusion (n = 7 each). Hepatic ischemia–reperfusion injury was induced by infrarenal abdominal aortic cross clamping for 60 min followed by 120 min of reperfusion. Fluoxetine (20 mg/kg/day, intraperitoneal) was administered for three consecutive days prior to ischemia. Oxidative stress markers, antioxidant parameters, inflammatory and anti-inflamma tory cytokines, apoptotic markers, and specific tissue injury biomarkers were measured in liver homogenates using ELISA. Histopathological alterations were evaluated by light microscopy. Ischemia–reperfusion significantly increased oxidant markers, inflammatory cytokines, NF-κB activation, apoptotic indices, liver enzyme levels, and histological damage, while reducing antioxidant capacity. Fluoxetine treatment markedly restored antioxidant defenses, suppressed oxidative stress, inflammation, apoptosis, and microcirculatory injury, and significantly improved histopathological findings compared with the untreated ischemia–reperfusion group. Fluoxetine exerts a protective effect against hepatic ischemia–reperfusion injury through antioxidant, anti-inflammatory and antiapoptotic mechanisms, suggesting its potential as a therapeutic agent in conditions associated with hepatic ischemia–reperfusion.
dc.identifier.citationIşık, M., Şahin, G., Kervancıoğlu, G., Güner, İ., Yaman, M. O., & Yelmen, N. (2026). Fluoxetine attenuates hepatic ischemia–reperfusion injury through antioxidant, anti‑inflammatory and anti‑apoptotic mechanisms. Naunyn-Schmiedeberg's Archives of Pharmacology, https://doi.org/10.1007/s00210-026-05563-8
dc.identifier.doi10.1007/s00210-026-05563-8
dc.identifier.issn1432-1912
dc.identifier.issn0028-1298
dc.identifier.pmidPMID: 42319415
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1007/s00210-026-05563-8
dc.identifier.urihttps://hdl.handle.net/20.500.13055/1519
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.indekslendigikaynak.otherSCI-E - Science Citation Index Expanded
dc.institutionauthorKervancıoğlu, Gülnaz
dc.institutionauthorid0000-0002-4737-3053
dc.language.isoen
dc.publisherSpringer Nature Link
dc.relation.ispartofNaunyn-Schmiedeberg's Archives of Pharmacology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectApoptosis
dc.subjectFluoxetine
dc.subjectHepatic Ischemia–Reperfusion Injury
dc.subjectInflammation
dc.subjectOxidative Stress
dc.titleFluoxetine attenuates hepatic ischemia–reperfusion injury through antioxidant, anti‑inflammatory and anti‑apoptotic mechanisms
dc.typeArticle
dspace.entity.typePublication

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