Protective Effect of Ramipril Against Oxidant and Proinflammatory Cytokine Damage Induced by Ischemia-Reperfusion in Ovarian Tissue in Rats

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Background: It is known that the increase in oxidants and proinflammatory cytokines, as well as the decrease in antioxidants, play a role in ovarian ischemia-reperfusion (I/R) injury. The antioxidant and anti-inflammatory properties of ramipril have been studied in various diseases. This study aims to investigate the effect of ramipril on I/R-induced ovarian damage in rats. Methods: Rats were divided into healthy (HG), sham (SG), ovary I/R (OIR), and ramipril + ovary I/R (ROIR) groups (n = 6/each group). One hour before the surgical procedures, ROIR was given 2 mg/kg ramipril. The lower abdomen of the SG, OIR, and ROIR was surgically opened. Right ovarian tissues of OIR and ROIR were subjected to 2 hours of ischemia and 6 hours of reperfusion. Then, all animals were euthanized, and their right ovaries were removed. Ovarian tissues were examined for oxidants (malondialdehyde), antioxidants (total glutathione, superoxide dismutase, and catalase), and proinflammatory cytokines (nuclear factor kappa-B, tumor necrosis factor-alpha, interleukin 1 beta, and interleukin-6) analysis was performed. Tissues were examined histopathologically. Results: The ovarian tissue of the OIR, which underwent the I/R procedure, exhibited a significant increase in oxidant and proinflammatory cytokine levels, along with a decrease in antioxidant levels (P < .001). Ramipril suppressed the I/R-induced increase in oxidants and pro-inflammatory cytokines and the decrease in antioxidants (P < .001). Ramipril also attenuated I/R-induced histopathological damage in ovarian tissue (P < .05). Conclusion: Ramipril treatment may be a treatment strategy to protect ovarian tissue against oxidative and inflammatory damage of I/R. © 2023 Elsevier Inc.

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AlanDeğerDil
dc.contributor.authorUlug, Pasa
dc.contributor.authorNayki, Umit
dc.contributor.authorMammadov, Renad
dc.contributor.authorBulut, Seval
dc.contributor.authorTastan, Tugba Bal
dc.contributor.authorCoban, Taha Abdulkadir
dc.contributor.authorSuleyman, Halis
dc.date.accessioned2026-10-18T20:26:50.001266122Z
dc.date.available2026-10-18T20:26:50.001266122Z
dc.date.issued2024
dc.description.abstractBackground: It is known that the increase in oxidants and proinflammatory cytokines, as well as the decrease in antioxidants, play a role in ovarian ischemia-reperfusion (I/R) injury. The antioxidant and anti-inflammatory properties of ramipril have been studied in various diseases. This study aims to investigate the effect of ramipril on I/R-induced ovarian damage in rats. Methods: Rats were divided into healthy (HG), sham (SG), ovary I/R (OIR), and ramipril + ovary I/R (ROIR) groups (n = 6/each group). One hour before the surgical procedures, ROIR was given 2 mg/kg ramipril. The lower abdomen of the SG, OIR, and ROIR was surgically opened. Right ovarian tissues of OIR and ROIR were subjected to 2 hours of ischemia and 6 hours of reperfusion. Then, all animals were euthanized, and their right ovaries were removed. Ovarian tissues were examined for oxidants (malondialdehyde), antioxidants (total glutathione, superoxide dismutase, and catalase), and proinflammatory cytokines (nuclear factor kappa-B, tumor necrosis factor-alpha, interleukin 1 beta, and interleukin-6) analysis was performed. Tissues were examined histopathologically. Results: The ovarian tissue of the OIR, which underwent the I/R procedure, exhibited a significant increase in oxidant and proinflammatory cytokine levels, along with a decrease in antioxidant levels (P < .001). Ramipril suppressed the I/R-induced increase in oxidants and pro-inflammatory cytokines and the decrease in antioxidants (P < .001). Ramipril also attenuated I/R-induced histopathological damage in ovarian tissue (P < .05). Conclusion: Ramipril treatment may be a treatment strategy to protect ovarian tissue against oxidative and inflammatory damage of I/R. © 2023 Elsevier Inc.
dc.identifier.doi10.1016/j.transproceed.2023.11.016
dc.identifier.eissn1873-2623
dc.identifier.endpage222
dc.identifier.issn0041-1345
dc.identifier.issue1
dc.identifier.pmid38218697
dc.identifier.scopus2-s2.0-85182568884
dc.identifier.startpage215
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/11836
dc.identifier.volume56
dc.identifier.wosWOS:001188078600001
dc.language.isoen
dc.publisherElsevier Inc.
dc.relation.ispartofTransplantation Proceedings
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectAnimals
dc.subjectAntioxidants
dc.subjectCytokines
dc.subjectFemale
dc.subjectIschemia
dc.subjectMalondialdehyde
dc.subjectOxidants
dc.subjectOxidative Stress
dc.subjectRamipril
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectReperfusion
dc.subjectReperfusion Injury
dc.subjectcatalase
dc.subjectglutathione
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectinterleukin 1beta
dc.subjectinterleukin 6
dc.subjectmalonaldehyde
dc.subjectsuperoxide dismutase
dc.subjecttumor necrosis factor
dc.subjectantioxidant
dc.subjectcytokine
dc.subjectoxidizing agent
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectantiinflammatory activity
dc.subjectantioxidant activity
dc.subjectArticle
dc.titleProtective Effect of Ramipril Against Oxidant and Proinflammatory Cytokine Damage Induced by Ischemia-Reperfusion in Ovarian Tissue in Rats
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus5
rdl.citation.wos5
rdl.departmentDepartment of Gynecology and Obstetrics, School of Medicine, Erzincan Binali Yıldırım University, Erzincan, Turkey. Electronic address: pasaulug@hotmail.com. | Department of Gynecology and Obstetrics, School of Medicine, Erzincan Binali Yıldırım University, Erzincan, Turkey. | Department of Pharmacology, School of Medicine, Erzincan Binali Yıldırım University, Erzincan, Turkey. | Department of Histology and Embryology, School of Medicine, Erzincan Binali Yıldırım University, Erzincan, Turkey. | Department of Medical Biochemistry, School of Medicine, Erzincan Binali Yıldırım University, Erzincan, Turkey.
rdl.oa.statusgold
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.source.indexPUBMED
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)