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Evaluation of the protective effects of gossypin for ischemia/reperfusion injury in ovary tissue

dc.contributor.authorDincer, Busra
dc.contributor.authorCinar, Irfan
dc.contributor.authorYayla, Muhammed
dc.contributor.authorToktay, Erdem
dc.date.accessioned2026-01-04T16:03:13Z
dc.date.issued2021-12-21
dc.description.abstractAbstractAimOvarian ischemia–reperfusion (I/R) injury is a serious gynecological condition that affects women of reproductive age and reduces ovarian reserve. Management of I/R injury with detorsion causes reperfusion damage, in which oxidative stress plays a central role. This study aimed to investigate whether the gossypin (GOS) with antioxidant properties, a flavonoid, has beneficial effects on the biochemical, molecular, and histopathological aspects of ovarian I/R injury.MethodsThirty‐three female Balb/c mice were randomly divided into five groups as follows: Healthy (Sham‐operated control group), I/R (IR group), I/R + GOS 5 (I/R with GOS 5 mg/kg), I/R + GOS 10 (I/R with GOS 10 mg/kg), and I/R + GOS 20 (I/R with GOS 20 mg/kg). This was followed by 3 h of ischemia and subsequent reperfusion for 3 h after detorsion was exposed. GOS was injected 2 h before reperfusion.ResultsIL‐1β, IL‐6, TNF‐α, NF‐κB, and CASP‐3 mRNA expressions, SOD (superoxide dismutase) activity, GSH (glutathione), and MDA (malondialdehyde) levels, and histopathological changes were evaluated in ovarian tissue. Histological examination indicated that treatment of ovarian I/R injury with GOS led to the improvement of ovarian tissue, which was accompanied by an increase in SOD activity and GSH level and a decrease in MDA level, NF‐κB, TNF‐α, IL‐1β, and IL‐6 expressions. GOS was also corrected by reducing the elevated expression of CASP‐3 as apoptosis‐change marker.ConclusionThese findings indicate that the treatment of GOS may be useful as a conservative approach to reverse I/R injury via amelioration of oxidative stress parameters and histopathological scores, attenuation of inflammation, and the suppression of apoptosis.
dc.description.urihttps://doi.org/10.1111/jog.15127
dc.description.urihttps://pubmed.ncbi.nlm.nih.gov/34931736
dc.identifier.doi10.1111/jog.15127
dc.identifier.eissn1447-0756
dc.identifier.endpage756
dc.identifier.issn1341-8076
dc.identifier.openairedoi_dedup___::59c374934659521001b7ff928a5a7377
dc.identifier.orcid0000-0002-3365-7741
dc.identifier.orcid0000-0002-0659-3084
dc.identifier.pubmed34931736
dc.identifier.scopus2-s2.0-85121466469
dc.identifier.startpage748
dc.identifier.urihttps://hdl.handle.net/20.500.12597/39241
dc.identifier.volume48
dc.identifier.wos000731912000001
dc.language.isoeng
dc.publisherWiley
dc.relation.ispartofJournal of Obstetrics and Gynaecology Research
dc.rightsCLOSED
dc.subjectFlavonoids
dc.subjectOvary
dc.subjectAntioxidants
dc.subjectRats
dc.subjectMice
dc.subjectOxidative Stress
dc.subjectIschemia
dc.subjectMalondialdehyde
dc.subjectReperfusion Injury
dc.subjectAnimals
dc.subjectFemale
dc.subjectRats, Wistar
dc.subject.sdg3. Good health
dc.titleEvaluation of the protective effects of gossypin for ischemia/reperfusion injury in ovary tissue
dc.typeArticle
dspace.entity.typePublication
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Management of I/R injury with detorsion causes reperfusion damage, in which oxidative stress plays a central role. This study aimed to investigate whether the gossypin (GOS) with antioxidant properties, a flavonoid, has beneficial effects on the biochemical, molecular, and histopathological aspects of ovarian I/R injury.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Thirty‐three female Balb/c mice were randomly divided into five groups as follows: Healthy (Sham‐operated control group), I/R (IR group), I/R + GOS 5 (I/R with GOS 5 mg/kg), I/R + GOS 10 (I/R with GOS 10 mg/kg), and I/R + GOS 20 (I/R with GOS 20 mg/kg). This was followed by 3 h of ischemia and subsequent reperfusion for 3 h after detorsion was exposed. GOS was injected 2 h before reperfusion.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:italic>IL‐1β, IL‐6, TNF‐α, NF‐κB</jats:italic>, and <jats:italic>CASP‐3</jats:italic> mRNA expressions, SOD (superoxide dismutase) activity, GSH (glutathione), and MDA (malondialdehyde) levels, and histopathological changes were evaluated in ovarian tissue. Histological examination indicated that treatment of ovarian I/R injury with GOS led to the improvement of ovarian tissue, which was accompanied by an increase in SOD activity and GSH level and a decrease in MDA level, <jats:italic>NF‐κB, TNF‐α, IL‐1β</jats:italic>, and <jats:italic>IL‐6</jats:italic> expressions. GOS was also corrected by reducing the elevated expression of <jats:italic>CASP‐3</jats:italic> as apoptosis‐change marker.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>These findings indicate that the treatment of GOS may be useful as a conservative approach to reverse I/R injury via amelioration of oxidative stress parameters and histopathological scores, attenuation of inflammation, and the suppression of apoptosis.</jats:p></jats:sec>"],"publicationDate":"2021-12-21","publisher":"Wiley","embargoEndDate":null,"sources":["Crossref"],"formats":null,"contributors":null,"coverages":null,"bestAccessRight":{"code":"c_14cb","label":"CLOSED","scheme":"http://vocabularies.coar-repositories.org/documentation/access_rights/"},"container":{"name":"Journal of Obstetrics and Gynaecology Research","issnPrinted":"1341-8076","issnOnline":"1447-0756","issnLinking":null,"ep":"756","iss":null,"sp":"748","vol":"48","edition":null,"conferencePlace":null,"conferenceDate":null},"documentationUrls":null,"codeRepositoryUrl":null,"programmingLanguage":null,"contactPeople":null,"contactGroups":null,"tools":null,"size":null,"version":null,"geoLocations":null,"id":"doi_dedup___::59c374934659521001b7ff928a5a7377","originalIds":["10.1111/jog.15127","50|doiboost____|59c374934659521001b7ff928a5a7377","34931736"],"pids":[{"scheme":"doi","value":"10.1111/jog.15127"},{"scheme":"pmid","value":"34931736"}],"dateOfCollection":null,"lastUpdateTimeStamp":null,"indicators":{"citationImpact":{"citationCount":11,"influence":2.98995e-9,"popularity":1.0281794e-8,"impulse":7,"citationClass":"C5","influenceClass":"C5","impulseClass":"C4","popularityClass":"C4"}},"instances":[{"pids":[{"scheme":"doi","value":"10.1111/jog.15127"}],"license":"Wiley Online Library User Agreement","type":"Article","urls":["https://doi.org/10.1111/jog.15127"],"publicationDate":"2021-12-21","refereed":"peerReviewed"},{"pids":[{"scheme":"pmid","value":"34931736"}],"alternateIdentifiers":[{"scheme":"doi","value":"10.1111/jog.15127"}],"type":"Article","urls":["https://pubmed.ncbi.nlm.nih.gov/34931736"],"publicationDate":"2022-03-04","refereed":"nonPeerReviewed"}],"isGreen":false,"isInDiamondJournal":false}
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