<?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>2026-10-19T06:00:33Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/14735" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/14735</identifier><datestamp>2026-10-18T21:14:24Z</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>Effect of Kineret® on ovarian ischemia reperfusion injury in a rat model</dc:title><dc:creator>Nayki, Umit Arslan</dc:creator><dc:creator>Nayki, Cenk</dc:creator><dc:creator>Cetin, Nihal</dc:creator><dc:creator>Cimen, Ferda Keskin</dc:creator><dc:creator>Coban, Abdulkadir</dc:creator><dc:creator>Mammadov, Renad</dc:creator><dc:creator>Tas, Ismail Hakkı</dc:creator><dc:creator>Malkoc, Ismail</dc:creator><dc:subject>apoptosis</dc:subject><dc:subject>IL-1β</dc:subject><dc:subject>ischemia/reperfusion</dc:subject><dc:subject>kineret</dc:subject><dc:subject>ovary</dc:subject><dc:subject>rat</dc:subject><dc:subject>Animals</dc:subject><dc:subject>Anti-Inflammatory Agents</dc:subject><dc:subject>Antioxidants</dc:subject><dc:subject>Caspase 3</dc:subject><dc:subject>Disease Models, Animal</dc:subject><dc:subject>Female</dc:subject><dc:subject>Gene Expression</dc:subject><dc:subject>Glutathione</dc:subject><dc:subject>Interleukin 1 Receptor Antagonist Protein</dc:subject><dc:subject>Interleukin-1beta</dc:subject><dc:subject>Malondialdehyde</dc:subject><dc:subject>Peroxidase</dc:subject><dc:subject>Rats</dc:subject><dc:subject>Rats, Wistar</dc:subject><dc:subject>Reperfusion Injury</dc:subject><dc:subject>complementary DNA</dc:subject><dc:subject>interleukin 1beta</dc:subject><dc:subject>malonaldehyde</dc:subject><dc:subject>myeloperoxidase</dc:subject><dc:subject>recombinant interleukin 1 receptor blocking agent</dc:subject><dc:subject>antiinflammatory agent</dc:subject><dc:subject>antioxidant</dc:subject><dc:subject>Casp3 protein, rat</dc:subject><dc:subject>interleukin 1 receptor blocking agent</dc:subject><dc:description>Aim: To investigate the effect of Kineret® on ischemia reperfusion (IR) injury in rat ovaries. Methods: Rats were divided into four groups: ovarian IR (IRG); 50 mg/kg Kineret® + ovarian IR (KIR-50); 100 mg/kg Kineret® + ovarian IR (KIR-100); and sham operation (SOC). KIR-50 (n = 10) and KIR-100 (n = 10) groups received an intraperitoneal injection of Kineret® at doses of 50 and 100 mg/kg, respectively. IRG and SOC (n = 10) rat groups were given distilled water as solvent using the same method. The results were compared between the groups. Results: In rats in which IR occurred, oxidant parameters, such as malondialdehyde (MDA) and myeloperoxidase (MPO), were increased, the level of proinflammatory interleukin 1 beta (IL-1β) was elevated and total glutathione (tGSH) as an antioxidant was decreased in the ovarian tissues. Administration of Kineret® at a dose of 100 mg/kg inhibited the increase of MDA, MOP and IL-1β and a decrease in tGSH caused by IR more significantly than administration of Kineret® at a dose of 50 mg/kg. In addition, 100 mg/kg Kineret® significantly decreased severe hemorrhage, degeneration and inflammatory signs in the follicular cells, caused by IR. Kineret® at 100 mg/kg markedly ameliorated increased apoptosis in ovarian tissue with IR more significantly than 50 mg/kg kineret. Conclusion: Our findings indicate that Kineret® might be useful in clinical practice for the treatment of damage that may occur as a result of ovarian torsion. © 2016 Japan Society of Obstetrics and Gynecology</dc:description><dc:publisher>Blackwell Publishing</dc:publisher><dc:date>2016</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/14735</dc:identifier><dc:identifier>https://doi.org/10.1111/jog.13095</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/14735</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>