Carvacrol treatment opens Kir6.2 ATP-dependent potassium channels and prevents apoptosis on rat testis following ischemia-reperfusion injury model

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dc.authorid0000-0002-3481-2782en_US
dc.authorid0000-0002-8317-7092en_US
dc.contributor.authorBalcı, Cemre Nur
dc.contributor.authorFırat, Tülin
dc.contributor.authorAcar, Nuray
dc.contributor.authorKükner, Aysel
dc.date.accessioned2023-05-12T08:35:38Z
dc.date.available2023-05-12T08:35:38Z
dc.date.issued2021en_US
dc.departmentBAİBÜ, Tıp Fakültesi, Temel Tıp Bilimleri Bölümüen_US
dc.description.abstractTesticular torsion is a urological problem that causes subfertility and testicular damage in males. Testis torsion and detorsion lead to ischemia– reperfusion (IR) injury in the testis. Testicular IR injury causes the increase of reactive oxygen species (ROS), oxidative stress (OS) and germ cell-specific apoptosis. In this study, we aimed to investigate whether Carvacrol has a protective effect on testicular IR injury and its effects on Kir6.2 channels, which is a member of adenosine triphosphate (ATP)-dependent potassium channels. In the study, 2–4 months old 36 albino Wistar rats were used. For experimental testicular IR model, the left testis was rotated counterclockwise at 720º for two hours, and after two hours following torsion, detorsion was performed. Carvacrol was dissolved in 5% Dimethyl Sulfoxide (DMSO) at a dose of 73 mg/kg and half an hour before detorsion, 0.2 mL was administered intraperitoneally. In testicular tissues, caspase 3 and Kir6.2 immunoexpressions were examined. Serum malondialdehyde (MDA) and testosterone levels were measured. Apoptotic cells and serum MDA levels were significantly decreased and Kir6.2 activation was significantly increased in Carvacrol-administrated IR group. As a result of our study, Carvacrol may activates Kir6.2 channels and inhibits apoptosis and may have a protective effect on testicular IR injury.en_US
dc.identifier.citationBalci, C. N., Firat, T., Acar, N., & Kukner, A. (2021). Carvacrol treatment opens Kir6. 2 ATP-dependent potassium channels and prevents apoptosis on rat testis following ischemia–reperfusion injury model. Romanian Journal of Morphology and Embryology, 62(1), 179.en_US
dc.identifier.doi10.47162/RJME.62.1.17
dc.identifier.endpage191en_US
dc.identifier.issn1220-0522
dc.identifier.issn2066-8279
dc.identifier.issue1en_US
dc.identifier.pmid34609420en_US
dc.identifier.scopus2-s2.0-85116972733en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage179en_US
dc.identifier.urihttp://dx.doi.org/10.47162/RJME.62.1.17
dc.identifier.urihttps://hdl.handle.net/20.500.12491/10875
dc.identifier.volume62en_US
dc.identifier.wosWOS:000704446600017en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.institutionauthorFırat, Tülin
dc.language.isoenen_US
dc.publisherEDITURA ACAD ROMANEen_US
dc.relation.ispartofRomanian Journal Of Morphology And Emiryologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectCarvacrolen_US
dc.subjectTestisen_US
dc.subjectIschemia–reperfusion injuryen_US
dc.subjectKir6.2en_US
dc.subjectCaspase 3en_US
dc.titleCarvacrol treatment opens Kir6.2 ATP-dependent potassium channels and prevents apoptosis on rat testis following ischemia-reperfusion injury modelen_US
dc.typeArticleen_US

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