<?xml version="1.0" encoding="UTF-8"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-10-18T23:54:16Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/12941" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/12941</identifier><datestamp>2026-10-18T21:13:25Z</datestamp><setSpec>openaire</setSpec><setSpec>driver</setSpec><setSpec>com_ebyu_10000</setSpec><setSpec>col_ebyu_10001</setSpec></header><metadata><oai_dc:dc xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"><dc:title>Evaluation of the protective effects of gossypin for ischemia/reperfusion injury in ovary tissue</dc:title><dc:creator>Dincer, Busra</dc:creator><dc:creator>Cinar, Irfan</dc:creator><dc:creator>Yayla, Muhammed</dc:creator><dc:creator>Toktay, Erdem</dc:creator><dc:subject>gossypin</dc:subject><dc:subject>inflammation</dc:subject><dc:subject>ischemia–reperfusion</dc:subject><dc:subject>ovary</dc:subject><dc:subject>oxidative stress</dc:subject><dc:subject>Animals</dc:subject><dc:subject>Antioxidants</dc:subject><dc:subject>Female</dc:subject><dc:subject>Flavonoids</dc:subject><dc:subject>Ischemia</dc:subject><dc:subject>Malondialdehyde</dc:subject><dc:subject>Mice</dc:subject><dc:subject>Rats</dc:subject><dc:subject>Rats, Wistar</dc:subject><dc:subject>Reperfusion Injury</dc:subject><dc:subject>caspase 3</dc:subject><dc:subject>glutathione</dc:subject><dc:subject>gossypine</dc:subject><dc:subject>immunoglobulin enhancer binding protein</dc:subject><dc:subject>interleukin 1beta</dc:subject><dc:subject>interleukin 6</dc:subject><dc:subject>malonaldehyde</dc:subject><dc:subject>messenger RNA</dc:subject><dc:subject>superoxide dismutase</dc:subject><dc:subject>tumor necrosis factor</dc:subject><dc:subject>antioxidant</dc:subject><dc:subject>flavonoid</dc:subject><dc:subject>animal experiment</dc:subject><dc:subject>animal model</dc:subject><dc:subject>animal tissue</dc:subject><dc:description>Aim: Ovarian 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. Methods: 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. Results: IL-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. Conclusion: 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. © 2021 Japan Society of Obstetrics and Gynecology.</dc:description><dc:publisher>John Wiley and Sons Inc</dc:publisher><dc:date>2022</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/12941</dc:identifier><dc:identifier>https://doi.org/10.1111/jog.15127</dc:identifier><dc:identifier>1341-8076</dc:identifier><dc:language>en</dc:language><dc:relation>Journal of Obstetrics and Gynaecology Research</dc:relation><dc:rights>info:eu-repo/semantics/openAccess</dc:rights><dc:type>info:eu-repo/semantics/article</dc:type><dc:identifier>https://ebyu-rdlopen.rawdatalibrary.net/tr/items/ebyu/12941</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>