Inhibition of c-jun n-terminal kinase attenuates diabetic testicular damage via endoplasmic reticulum stress reduction

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dc.authorid0000-0003-4785-4751
dc.authorid0000-0001-9829-7903
dc.authorid0000-0002-2353-1184
dc.authorid0000-0003-1793-7003
dc.contributor.authorBayram, Şinasi
dc.contributor.authorErsoy, Onur
dc.contributor.authorDeveci, Engin
dc.contributor.authorKızılay, Gülnur
dc.date.accessioned2026-06-25T13:32:55Z
dc.date.available2026-06-25T13:32:55Z
dc.date.issued2026
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Histoloji ve Embriyoloji Ana Bilim Dalı
dc.description.abstractThe underlying causes of many diabetes-related complications are well known. However, the reasons for the complication related to male reproductive health remain unclear. Hyperglycemia disrupts the balance between oxidants and antioxidants, causing damage to cells, especially ER stress. ER stress triggered by the proteins accumulating in the ER lumen causes apoptosis by activating various pathways. c-Jun N-terminal kinase (JNK) is a key protein in systemic diseases like diabetes, and SP600125 is a widely used JNK inhibitor. This study focuses on whether JNK inhibition by SP600125 prevents diabetic testicular damage by reducing ER stress. In our study, animals were divided into three groups: Control group, the diabetes group, and the JNK inhibition group. Blood glucose level, body and testicular weights, and seminiferous tubule diameters were measured. Seminiferous tubules were evaluated by the Johnsen score in Hematoxyline and Eosin stained sections. Protein expressions of caspase 3, phospho (p)-JNK, caspase 12, and CHOP were evaluated. The Inhibitor group had significantly decreased active caspase-3, (p)-JNK, caspase-12, CHOP values, and blood glucose levels, increased body and testicular weights, seminiferous tubule diameter, and Johnsen score values compared to the diabetes group. JNK inhibition significantly ameliorated the histopathological damage in testicular tissue by preventing diabetes-induced ER stress and apoptosis.
dc.identifier.citationBayram, Ş., Ersoy, O., Deveci, E., & Kızılay, G. (2026). Inhibition of c-jun n-terminal kinase attenuates diabetic testicular damage via endoplasmic reticulum stress reduction. International Journal of Morphology, 44(2), pp. 683-689. http://dx.doi.org/10.4067/s0717-95022026000200683
dc.identifier.doi10.4067/s0717-95022026000200683
dc.identifier.endpage689
dc.identifier.issn0717-9367
dc.identifier.issn0717-9502
dc.identifier.issue2
dc.identifier.scopus2-s2.0-105044771068
dc.identifier.scopusqualityQ3
dc.identifier.startpage683
dc.identifier.urihttp://dx.doi.org/10.4067/s0717-95022026000200683
dc.identifier.urihttps://hdl.handle.net/20.500.13055/1518
dc.identifier.volume44
dc.identifier.wosWOS:001824919600040
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.indekslendigikaynak.otherSCI-E - Science Citation Index Expanded
dc.institutionauthorBayram, Şinasi
dc.institutionauthorid0000-0003-4785-4751
dc.language.isoen
dc.publisherUniversidad de la Frontera
dc.relation.ispartofInternational Journal of Morphology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectDiabetes Mellitus
dc.subjectProtein Kinase Inhibitors
dc.subjectEndoplasmic Reticulum Stress
dc.subjectApoptosis
dc.subjectTestis
dc.titleInhibition of c-jun n-terminal kinase attenuates diabetic testicular damage via endoplasmic reticulum stress reduction
dc.typeArticle
dspace.entity.typePublication

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