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dc.contributor.authorSever, I. H.
dc.contributor.authorOzkul, B.
dc.contributor.authorErisik Tanriover, D.
dc.contributor.authorOzkul, O.
dc.contributor.authorElgormus, C. S.
dc.contributor.authorGur, S. G.
dc.contributor.authorSogut, I.
dc.date.accessioned2022-01-29T16:52:19Z
dc.date.available2022-01-29T16:52:19Z
dc.date.issued2021
dc.identifier.issn0190-2148
dc.identifier.issn1521-0499
dc.identifier.urihttps://doi.org/10.1080/01902148.2021.1992808
dc.identifier.urihttp://hdl.handle.net/11446/4427
dc.description.abstractPurpose: Although several studies demonstrate the anti-inflammatory effect of oxytocin in different pathophysiological processes, there are limited data describing the impact of oxytocin on acute respiratory distress syndrome (ARDS). We aimed to elucidate the protective effect of oxytocin in ARDS with histopathological evaluation and radiological imaging in addition to biochemical markers. Materials and Methods: Fecal intraperitoneal injection procedure (FIP) was performed on 24 of 32 rats included in the study for creating a sepsis model. Rats were randomly assigned into four groups: control group (no procedure was applied, n = 8), untreated septic group [was operated (FIP) and received no treatment, n = 8], placebo group (FIP, treated with 10 ml/kg of saline at once, n = 8), and treated group (FIP, treated with 0.1 mg/kg of oxytocin at once, n = 8). Chest CT was performed for all rats 20 hours after the procedure and density of the lungs were measured manually by using HU. All animals were sacrificed for histopathological examination of lung damage and blood samples were collected for biochemical analysis. Results: Plasma malondialdehyde (MDA), lactic acid (LA), C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), interleukin 1-beta (IL 1-beta) levels were significantly increased in the placebo (FIP + saline) and the untreated (FIP) groups, and plasma levels of all biomarkers were reversed by oxytocin. Further, the density of the lung parenchyma (Hounsfield unit) on CT images and the histopathological lung damage score values were closer to the control group in the oxytocin-treated group compared to the placebo group. Conclusion: Our findings suggested that oxytocin could exert anti-inflammatory, antioxidant and protective effects in FIP-induced ARDS.en_US
dc.language.isoengen_US
dc.publisherTaylor & Francis Incen_US
dc.identifier.doi10.1080/01902148.2021.1992808
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAcute lung injuryen_US
dc.subjectARDSen_US
dc.subjectcomputerized tomographyen_US
dc.subjectinflammationen_US
dc.subjectoxytocinen_US
dc.subjectoxidationen_US
dc.subjectRespiratory-Distress-Syndromeen_US
dc.subjectIschemia-Reperfusion Injuryen_US
dc.subjectMechanismsen_US
dc.subjectMortalityen_US
dc.subjectRatsen_US
dc.titleProtective effect of oxytocin through its anti-inflammatory and antioxidant role in a model of sepsis-induced acute lung injury: Demonstrated by CT and histological findingsen_US
dc.typearticleen_US
dc.relation.journalExperimental Lung Researchen_US
dc.departmentDBÜen_US
dc.identifier.issue9en_US
dc.identifier.volume47en_US
dc.identifier.startpage426en_US
dc.identifier.endpage435en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.department-temp[Sever, I. H.; Gur, S. G.] Demiroglu Bilim Univ, Dept Radiol, Abide I Hurriyet St 166, TR-34381 Istanbul, Turkey; [Ozkul, B.] Istanbul Atlas Univ, Dept Radiol, Istanbul, Turkey; [Erisik Tanriover, D.; Uyanikgil, Y.] Ege Univ, Fac Med, Dept Histol & Embryol, Izmir, Turkey; [Ozkul, O.] Bagcilar Res & Training Hosp, Med Oncol, Istanbul, Turkey; [Elgormus, C. S.] Istanbul Atlas Univ, Dept Emergency Med, Istanbul, Turkey; [Sogut, I.] Demiroglu Bilim Univ, Dept Biochem, Istanbul, Turkey; [Cetin, E. O.] Ege Univ, Dept Biopharmaceut & Pharmacokinet, Dept Pharmaceut Technol, Fac Pharm, Izmir, Turkey; [Erbas, O.] Demiroglu Bilim Univ, Dept Physiol, Istanbul, Turkeyen_US
dc.authoriduyanikgil, Yigit/0000-0002-4016-0522
dc.authorwosiduyanikgil, Yigit/M-2746-2019


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