Antithrombin Prevents Apoptosis by Regulating Inflammation in the Liver in a Model of Cold Ischemia/Warm Reperfusion Injury

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dc.authoridDEMIRBAG, Ali E./0000-0003-3852-868X
dc.authorwosidDEMIRBAG, Ali E./AAA-4186-2021
dc.contributor.authorIsik, Sevil
dc.contributor.authorTuncyurek, Pars
dc.contributor.authorZengin, Neslihan Inci
dc.contributor.authorDemirbag, Ali Eba
dc.contributor.authorAtalay, Fuat
dc.contributor.authorYilmaz, Sezai
dc.contributor.authorOrug, Taner
dc.date.accessioned2024-08-04T20:35:52Z
dc.date.available2024-08-04T20:35:52Z
dc.date.issued2012
dc.departmentİnönü Üniversitesien_US
dc.description.abstractBackground/Aims: Hepatic ischemia-reperfusion injury is a major problem in liver surgery. To modulate the complex process of inflammation, additional drugs to add to well-defined organ preserving solutions have been sought. The aim of the current study was: to investigate the additive potential of antithrombin (AT) in liver preservation. Methodology: Female Wistar rats were randomized into four groups: sham (Group I), experiment model (Group II), and treatment groups with AT (250U/kg) administration systematically (Group III) or locally (Group IV) before hepatectomy. UW solution was used for liver preservation for 24h at 4 degrees C. The livers in group II, III and IV were reperfused 1h and histopathological parameters were evaluated microscopically. Apoptosis was assessed with TUNEL test. Results: Karyorrhexis was lower in the local treatment with AT group. Sinusoidal desquamation and mononuclear cell infiltration was higher in the experimental model group. Sinusoidal enlargement was higher in the systemic AT treatment group and neutrophil infiltration to sinusoids was lowest in the local treatment group. Apoptosis of hepatocytes and sinusoidal cells were significantly suppressed in rats that were treated with AT via portal vein infusion. Conclusions: AT treatment obviously contributed to liver preservation in our model; the effects on apoptosis and inflammation were prominent. Therefore, AT should be considered as a potent agent although its clinical role has yet to be defined in ex-vivo hepatic preservation.en_US
dc.identifier.doi10.5754/hge11317
dc.identifier.endpage457en_US
dc.identifier.issn0172-6390
dc.identifier.issue114en_US
dc.identifier.pmid21940387en_US
dc.identifier.scopus2-s2.0-84860598180en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage453en_US
dc.identifier.urihttps://doi.org/10.5754/hge11317
dc.identifier.urihttps://hdl.handle.net/11616/95643
dc.identifier.volume59en_US
dc.identifier.wosWOS:000303101300037en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherH G E Update Medical Publishing S Aen_US
dc.relation.ispartofHepato-Gastroenterologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAntithrombinen_US
dc.subjectIschemia/reperfusion injuryen_US
dc.subjectLiver preservationen_US
dc.titleAntithrombin Prevents Apoptosis by Regulating Inflammation in the Liver in a Model of Cold Ischemia/Warm Reperfusion Injuryen_US
dc.typeArticleen_US

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