Regression of experimental endometriotic implants in a rat model with the angiotensin II receptor blocker losartan

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dc.contributor.authorCakmak, Bulent
dc.contributor.authorCavusoglu, Turker
dc.contributor.authorAtes, Utku
dc.contributor.authorMeral, Ayfer
dc.contributor.authorNacar, Mehmet Can
dc.contributor.authorErbas, Oytun
dc.date.accessioned2019-10-27T19:53:57Z
dc.date.available2019-10-27T19:53:57Z
dc.date.issued2015
dc.departmentEge Üniversitesien_US
dc.description.abstractAimEndometriosis is a common disease in women of reproductive age, and many different treatments have been developed, although none has provided a cure. In this study, the efficacy of losartan, an angiotensin II type 1 receptor blocker and an antiangiogenic and anti-inflammatory agent, on regression of experimental endometriotic implants in a rat model was investigated. MethodsPeritoneal endometriosis was surgically induced in 16 mature female Sprague-Dawley rats. The peritoneal endometriotic implant was confirmed after 28 days, and the animals were divided randomly into two groups. The control group (n=8) was given 4mL/day tap water by oral gavage, and the losartan group (n=8) was given 20mg/kg per day losartan p.o. We compared endometriotic implant size, extent and severity of adhesion, as well as plasma and peritoneal lavage fluid cytokine levels including vascular endothelial growth factor (VEGF) and tumor necrosis factor (TNF)-, plasma inflammatory factor pentraxin-3 (PTX-3) and C-reactive protein (CRP) between the treatment groups. ResultsMean surface endometriotic area, histological score of implants, adhesion formation, plasma VEGF, TNF, PTX-3 and CRP levels were significantly lower in the losartan group compared with control (P<0.05). Furthermore, the peritoneal VEGF level was lower in the losartan group than in the control group (P<0.001), but peritoneal TNF- was similar in both groups (P>0.05). ConclusionLosartan suppressed the implant surface area of experimental endometriosis in rats and reduced the levels of plasma VEGF, TNF-, PTX-3 and CRP.en_US
dc.identifier.doi10.1111/jog.12558en_US
dc.identifier.endpage607en_US
dc.identifier.issn1341-8076
dc.identifier.issn1447-0756
dc.identifier.issue4en_US
dc.identifier.pmid25302540en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage601en_US
dc.identifier.urihttps://doi.org/10.1111/jog.12558
dc.identifier.urihttps://hdl.handle.net/11454/40392
dc.identifier.volume41en_US
dc.identifier.wosWOS:000352786800016en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofJournal of Obstetrics and Gynaecology Researchen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectangiogenic factorsen_US
dc.subjectangiotensin II receptor blockeren_US
dc.subjectendometriosisen_US
dc.subjectlosartanen_US
dc.subjectvascular endothelial growth factoren_US
dc.titleRegression of experimental endometriotic implants in a rat model with the angiotensin II receptor blocker losartanen_US
dc.typeArticleen_US

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