Melatonin attenuates oxidative stress, liver damage and hepatocyte apoptosis after bile-duct ligation in rats

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dc.authorscopusid24436194200
dc.authorscopusid7006356462
dc.authorscopusid36023238400
dc.authorscopusid36608599700
dc.authorscopusid55881189500
dc.authorwosidAktas, Cevat/D-8468-2011
dc.contributor.authorAktaş, Cevat
dc.contributor.authorKanter, Mehmet
dc.contributor.authorErboğa, Mustafa
dc.contributor.authorMete, Rafet
dc.contributor.authorOran, Mustafa
dc.date.accessioned2022-05-11T14:12:46Z
dc.date.available2022-05-11T14:12:46Z
dc.date.issued2014
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Histoloji ve Embriyoloji Ana Bilim Dalı
dc.departmentFakülteler, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, İç Hastalıkları Ana Bilim Dalı
dc.description.abstractThe goal of this study was to evaluate the possible protective effects of melatonin against cholestatic oxidative stress, liver damage and hepatocyte apoptosis in the common rats with bile duct ligation (BDL). A total of 24 male Wistar albino rats were divided into three groups: control, BDL and BDL + received melatonin; each group contains eight animals. Melatonin-treated BDL rats received daily melatonin 100 mg/kg/day via intraperitoneal injection. The application of BDL clearly increased the malondialdehyde (MDA) levels and decreased the superoxide dismutase (SOD) and glutathione (GSH) activities. Melatonin treatment significantly decreased the elevated tissue MDA levels and increased the reduced SOD and GSH enzyme levels in the tissues. The changes demonstrate that the bile duct proliferation and fibrosis in expanded portal tracts include the extension of proliferated bile ducts into lobules, mononuclear cells and neutrophil infiltration into the widened portal areas as observed in the BDL group. The data indicate that melatonin attenuates BDL-induced cholestatic liver injury, bile duct proliferation and fibrosis. The alpha-smooth muscle actin (alpha-SMA) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells in the BDL were observed to be reduced with the melatonin treatment. These results suggest that administration of melatonin is a potentially beneficial agent to reduce liver damage in BDL by decreasing oxidative stress.
dc.identifier.doi10.1177/0748233712464811
dc.identifier.endpage844
dc.identifier.issn0748-2337
dc.identifier.issn1477-0393
dc.identifier.issue9en_US
dc.identifier.pmid23095487
dc.identifier.scopus2-s2.0-84910035016
dc.identifier.scopusqualityQ3
dc.identifier.startpage835
dc.identifier.urihttps://doi.org/10.1177/0748233712464811
dc.identifier.urihttps://hdl.handle.net/20.500.11776/5668
dc.identifier.volume30
dc.identifier.wosWOS:000342991800007
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorAktaş, Cevat
dc.institutionauthorKanter, Mehmet
dc.institutionauthorErboğa, Mustafa
dc.institutionauthorMete, Rafet
dc.institutionauthorOran, Mustafa
dc.language.isoen
dc.publisherSage Publications Inc
dc.relation.ispartofToxicology and Industrial Health
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectBile duct ligation
dc.subjectliver
dc.subjectmelatonin
dc.subjectoxidative stress
dc.subjectapoptosis
dc.subjectalpha-sma
dc.subjectBiliary-Obstructed Rats
dc.subjectHepatic Stellate Cells
dc.subjectCarbon-Tetrachloride
dc.subjectFibrosis
dc.subjectPathogenesis
dc.subjectExpression
dc.subjectJaundice
dc.subjectInjury
dc.subjectInhibition
dc.subjectActivation
dc.titleMelatonin attenuates oxidative stress, liver damage and hepatocyte apoptosis after bile-duct ligation in rats
dc.typeArticle

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