Effect of trimetazidine against ovarian ischemia/reperfusion injury in rat model: A new pathway: JAK2/STAT3

dc.contributor.authorYuksel, Tugba Nurcan
dc.contributor.authorHalici, Zekai
dc.contributor.authorCadirci, Elif
dc.contributor.authorToktay, Erdem
dc.contributor.authorOzdemir, Bengul
dc.contributor.authorBozkurt, Ayse
dc.date.accessioned2024-10-29T17:59:01Z
dc.date.available2024-10-29T17:59:01Z
dc.date.issued2023
dc.departmentTekirdağ Namık Kemal Üniversitesi
dc.description.abstractObjective(s): Ovarian ischemia/reperfusion (I/R) is an extremely complex pathological problem that begins with oxygen deprivation, progresses to excessive free radical production, and intensifies inflammation. The JAK2/STAT3 signaling pathway is a multipurpose signaling transcript channel that plays a role in several biological functions. Trimetazidine (TMZ) is a cellular anti-ischemic agent. This study aims to investigate the effects of TMZ on ovarian I/R injury in rats. Materials and Methods: sixty four rats were divided into 8 groups at random: healthy(group1); healthy+TMZ20(group2); ischemia (I) (group 3); I+TMZ10(group4); I+ TMZ20(group5); I/R(group6); I/R+TMZ10(group7); I/R+TMZ20(group8). Vascular clamps were placed just beneath the ovaries and over the uterine horns for 3 hr to induce ischemia. The clamps were removed for the reperfusion groups, and the rats were reperfused with care to ensure that the blood flowed into the ovaries, subjecting them to reperfusion for 3 hr. TMZ was administered orally by gavage 6 and 1 hr before operations. At the end of the experiment, ovarian tissues were removed for biochemical, molecular, and histopathological investigation. Results: TMZ administration ameliorated ischemia/reperfusion-induced disturbances in GSH and MDA levels. TMZ treatment inhibited I/R-induced JAK2/STAT3 signaling pathway activation in ovarian tissues. TMZ administration also improved the increase in the mRNA expressions of IL1 beta, TNF-alpha, and NF-KB caused by ischemia/reperfusion injury. Moreover, TMZ treatment improved histopathologic injury in ovarian tissues caused by ischemia/reperfusion. Conclusion: TMZ treatment protected rats against ovarian ischemia/reperfusion injury by alleviating oxidative stress and inflammatory cascades. These findings may provide a mechanistic basis for using TMZ to treat ovarian ischemia-reperfusion injury.
dc.identifier.doi10.22038/IJBMS.2023.72544.15776
dc.identifier.endpage1379
dc.identifier.issn2008-3866
dc.identifier.issn2008-3874
dc.identifier.issue11en_US
dc.identifier.pmid37886007
dc.identifier.scopus2-s2.0-85179433170
dc.identifier.scopusqualityQ2
dc.identifier.startpage1370
dc.identifier.urihttps://doi.org/10.22038/IJBMS.2023.72544.15776
dc.identifier.urihttps://hdl.handle.net/20.500.11776/14593
dc.identifier.volume26
dc.identifier.wosWOS:001076539200015
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherMashhad Univ Med Sciences
dc.relation.ispartofIranian Journal of Basic Medical Sciences
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectIschemia
dc.subjectJAK2/STAT3
dc.subjectOxidative stress
dc.subjectOvary
dc.subjectReperfusion
dc.subjectTrimetazidine
dc.titleEffect of trimetazidine against ovarian ischemia/reperfusion injury in rat model: A new pathway: JAK2/STAT3
dc.typeArticle

Dosyalar