<?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>2026-10-19T01:43:54Z</responseDate><request verb="GetRecord" identifier="oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/13950" metadataPrefix="oai_dc">https://ebyu-rdlopen.rawdatalibrary.net/oai/request</request><GetRecord><record><header><identifier>oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/13950</identifier><datestamp>2026-10-18T21:14:21Z</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>The investigation of the protective effects of nimesulide on experimental testicular ischemia-reperfusion injury in rats; [La investigación de los efectos protectores de nimesulida en la lesión de isquemia y reperfusión testicular experimental en ratas]</dc:title><dc:creator>Polat, Eyüp Can</dc:creator><dc:creator>Bozkurt, Ali Seydi</dc:creator><dc:creator>Keskin Cimen, Ferda</dc:creator><dc:creator>Gulaboglu, Mine</dc:creator><dc:creator>Altuner, Durdu</dc:creator><dc:subject>Ischemia/reperfusion</dc:subject><dc:subject>Nimesulide</dc:subject><dc:subject>Testis</dc:subject><dc:subject>Animals</dc:subject><dc:subject>Anti-Inflammatory Agents, Non-Steroidal</dc:subject><dc:subject>Antioxidants</dc:subject><dc:subject>Cyclooxygenase Inhibitors</dc:subject><dc:subject>Dose-Response Relationship, Drug</dc:subject><dc:subject>Inflammation</dc:subject><dc:subject>Male</dc:subject><dc:subject>Oxidative Stress</dc:subject><dc:subject>Rats</dc:subject><dc:subject>Rats, Wistar</dc:subject><dc:subject>Reactive Oxygen Species</dc:subject><dc:subject>Reperfusion Injury</dc:subject><dc:subject>Spermatic Cord Torsion</dc:subject><dc:subject>Sulfonamides</dc:subject><dc:subject>antioxidant</dc:subject><dc:subject>nonsteroid antiinflammatory agent</dc:subject><dc:subject>prostaglandin synthase inhibitor</dc:subject><dc:subject>reactive oxygen metabolite</dc:subject><dc:subject>sulfonamide</dc:subject><dc:subject>animal</dc:subject><dc:subject>dose response</dc:subject><dc:subject>drug effect</dc:subject><dc:subject>metabolism</dc:subject><dc:subject>pathophysiology</dc:subject><dc:subject>rat</dc:subject><dc:subject>testis torsion</dc:subject><dc:subject>Wistar rat</dc:subject><dc:description>Introduction and objectives: Testicular ischemia/reperfusion (I/R) injury develops after torsion and following detorsion of the testis. Reactive oxygen species were produced and oxidative damage begins to occur due to I/R process. Nimesulide, which is a specific cyclooxygenase-2 inhibitor drug, have antioxidant, antiinflammatory, analgesics and antipyretic effects. We aimed to investigate biochemically and histopathologically effect of nimesulide on testis I/R injury in rats induced by the testicular torsion–detorsion. Material and methods: In this study, 24 albino Wistar male rats were divided into four groups (6 rats in each group): ischemia/reperfusion applied + 50 mg/kg nimesulide administrated (NIM-50), ischemia/reperfusion applied + 100 mg/kg nimesulide administrated (NIM-100), ischemia/reperfusion applied (IR) and Sham surgery (SS) groups. Nimesulide was administered to NIM-50 and NIM-100 groups at the 50 mg/kg and 100 mg/kg doses before 2 h applied I/R procedures. The IR group were applied only I/R procedures, no drug treatment was applied. Animals were sacrificed under high dose anesthesia and left testes were extracted. Testes were examined biochemically and histopathologically. Results: Total glutathione (tGSH) and cyclooxygenase-1 (COX-1) levels were increased in the NIM-50 and NIM-100 groups compared to IR group. The levels of COX-2, malondialdehyde (MDA), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) were lower in the NIM-50 and NIM-100 groups than in the IR group. Some histopathological changes seen in IR group. This findings were decreased in NIM-50 group and prevented in NIM-100 group. Conclusion: Nimesulide prevented inflammation and oxidative stress. Our results suggest that nimesulide may be have a protective effect on testicular I/R injury. © 2018 Asociación Española de Andrología, Medicina Sexual y Reproductiva</dc:description><dc:publisher>Ediciones Doyma, S.L.</dc:publisher><dc:date>2020</dc:date><dc:type>Article</dc:type><dc:identifier>https://rdlopen.rawdatalibrary.net/r/ebyu/13950</dc:identifier><dc:identifier>https://doi.org/10.1016/j.androl.2018.08.001</dc:identifier><dc:identifier>1698-031X</dc:identifier><dc:language>en</dc:language><dc:relation>Revista Internacional de Andrologia</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/13950</dc:identifier></oai_dc:dc></metadata></record></GetRecord></OAI-PMH>