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dc.contributor.authorAkkoyun, Dursun Çayan
dc.contributor.authorAkyüz, Aydın
dc.contributor.authorDoğan, Mustafa
dc.contributor.authorErboğa, Mustafa
dc.contributor.authorAktaş, Cevat
dc.contributor.authorÇağlar, Veli
dc.contributor.authorGürel, Ahmet
dc.date.accessioned2022-05-11T14:07:32Z
dc.date.available2022-05-11T14:07:32Z
dc.date.issued2016
dc.identifier.issn0884-6812
dc.identifier.urihttps://hdl.handle.net/20.500.11776/5139
dc.description.abstractOBJECTIVE: To examine the histopathological and biochemical effects of quercetin (QE), which has antioxidant properties, on damaged heart muscle in a lipopolysaccharide (LPS)-induced endotoxemia model in rats. STUDY DESIGN: Rats were divided into 4 groups: Control, QE, LPS, and LPS+QE. Escherichia coli LPS, 10 mg/kg, was administered intravenously to induce endotoxemia in the LPS and LPS+QE groups. A single dose of 50 mg/kg QE was administered intraperitoneally to QE groups 30 minutes prior to administering LPS. The rats were sacrificed at the end of the 6-hour period following LPS application. RESULTS: It was observed in histopathological evaluations that the heart tissue injury and inflammation in the LPS groups were higher than those of the LPS+QE group, and that QE partially prevented damage caused by endotoxemia. Rats in the LPS groups demonstrated significantly increased tissue malondialdehyde levels and significantly decreased enzymatic antioxidants superoxide dismutase and catalase in the cardiac tissue. It was observed that QE treatment increased the superoxide dismutase and catalase enzyme levels that decreased after LPS. CONCLUSION: QE with antioxidant properties prevented heart damage caused by free oxygen radicals that occurred after LPS-induced endotoxemia and increased the antioxidant defense system.en_US
dc.language.isoengen_US
dc.publisherSci Printers & Publ Incen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectantioxidant effecten_US
dc.subjectantioxidantsen_US
dc.subjectendotoxemiaen_US
dc.subjectendotoxinsen_US
dc.subjectflavonolen_US
dc.subjecthearten_US
dc.subjectlipoglycansen_US
dc.subjectlipopolysaccharidesen_US
dc.subjectLPSen_US
dc.subjectoxidative damageen_US
dc.subjectoxidative stressen_US
dc.subjectquercetinen_US
dc.subjectsepsisen_US
dc.subjectseptic shocken_US
dc.subjectshocken_US
dc.subjectendotoxicen_US
dc.subjecttoxemiaen_US
dc.subjectAcute Lung Injuryen_US
dc.subjectOxidative Stressen_US
dc.subjectSevere Sepsisen_US
dc.subjectSeptic Shocken_US
dc.subjectDysfunctionen_US
dc.subjectBioavailabilityen_US
dc.subjectInflammationen_US
dc.subjectMechanismsen_US
dc.subjectExpressionen_US
dc.subjectMortalityen_US
dc.titleQuercetin Inhibits Heart Injury in Lipopolysaccharide-induced Endotoxemic Model by Suppressing the Effects of Reactive Oxygen Speciesen_US
dc.typearticleen_US
dc.relation.ispartofAnalytical and Quantitative Cytopathology and Histopathologyen_US
dc.departmentFakülteler, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, Kardiyoloji Ana Bilim Dalıen_US
dc.departmentFakülteler, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, Enfeksiyon Hastalıkları Ana Bilim Dalıen_US
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Histoloji ve Embriyoloji Ana Bilim Dalıen_US
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Anatomi Ana Bilim Dalıen_US
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Biyoistatistik Ana Bilim Dalıen_US
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Tıbbi Biyokimya Ana Bilim Dalıen_US
dc.authorid0000-0002-2270-2965
dc.identifier.volume38en_US
dc.identifier.issue3en_US
dc.identifier.startpage183en_US
dc.identifier.endpage188en_US
dc.institutionauthorAkkoyun, Dursun Çayan
dc.institutionauthorAkyüz, Aydın
dc.institutionauthorDoğan, Mustafa
dc.institutionauthorErboğa, Mustafa
dc.institutionauthorAktaş, Cevat
dc.institutionauthorÇağlar, Veli
dc.institutionauthorGürel, Ahmet
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.authorwosidAktas, Cevat/D-8468-2011
dc.authorwosidYilmaz, Ahsen/ABB-1083-2021
dc.identifier.wosWOS:000399656100006en_US


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