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    Inhibition of c-jun n-terminal kinase attenuates diabetic testicular damage via endoplasmic reticulum stress reduction
    (Universidad de la Frontera, 2026) Bayram, Şinasi; Ersoy, Onur; Deveci, Engin; Kızılay, Gülnur
    The 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.
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    Protective effects of royal jelly in diabetic rat testis tissue through apoptotic and antiapoptotic pathways
    (Aves, 2026) Ersoy, Onur; Delen, Özlem; Yavaş, Şirin; Bayram, Şinasi; Kızılay, Gülnur
    Objective: Diabetic male subfertility and/or infertility represents an area of research that has attracted attention and therefore become a subject of investigation at the molecular level. The insulin-like effects, antihypertensive, antitumor, antioxidative, anti-inflammatory, and immunomodulatory roles of royal jelly (RJ) have been demonstrated by scientific research. This study was designed based on the hypothesis that RJ may have the potential to prevent apoptosis in testicular tissue and, consequently, exert a beneficial impact on spermatogenesis through its ability to mitigate the adverse effects of diabetes on testicular tissue. The aim is to identify some of the molecular factors that may be responsible for the therapeutic effects of RJ on diabetic testicular tissue. Methods: Apoptosis, proliferation, and Leydig cell functions were determined using the following markers: transferase dUTP nick end labeling analysis, c-Jun N-terminal kinase (JNK), p38, Fas, and FasL for apoptosis; proliferating cell nuclear antigen (PCNA) and extracellular signal-regulated kinase (ERK) for proliferation; and insulin-like peptide-3 (INSL3) for Leydig cell function. A total of 20 Wistar albino male rats were randomly assigned to 3 experimental groups. The control group (C) and the diabetic group (D) were administered a single dose of 50 mg/kg STZ (intraperitoneally), and the RJ group was given 400 mg/kg/day (ig.) RJ after a single dose of 50 mg/kg STZ. Results: While PCNA, ERK, and INSL3 immunoreactivities were significantly increased, the apoptotic cell and tubule indices, JNK, p38, Fas, and FasL immunoreactivities were significantly decreased in the RJ group compared to the D group. Conclusion: Royal jelly may have a protective effect in preventing diabetes-related male infertility through apoptosis and anti-apoptotic pathways.