Kizilay, GulnurBayram, SinasiErsoy, OnurCerkezkayabekir, AysegulSapmaz-Metin, MelikeKaraca, Turan2024-06-122024-06-1220221052-02951473-7760https://doi.org/10.1080/10520295.2021.2002931https://hdl.handle.net/20.500.14551/18243We investigated how proanthocyanidin treatment altered c-Jun N-terminal kinases, transforming growth factor beta 1, serine/threonine-specific protein kinase, interleukin 1 beta and insulin-like 3 expression in the testis of diabetic rats. We used 24 Wistar albino male rats divided into four groups. Group 1 was untreated control. Group 2 was treated with 40 mg/kg streptozotocin (STZ) for 5 days. Group 3 was treated with 40 mg/kg STZ + 250 mg/kg proanthocyanidin once daily for six weeks. Group 4 was treated with 40 mg/kg STZ + 250 mg/kg proanthocyanidin. Superoxide dismutase activity was reduced in groups 3 and 4 compared to group 2. Glutathione peroxidase activity was increased significantly in groups 3 and 4 compared to groups 1 and 2. Catalase activity was decreased in group 4 compared to group 2. We found that proanthocyanidin increased cell proliferation in diabetic testis. Phospho-JNK and TGF-beta 1 immunostaining was decreased groups 3 and 4 compared to group 2, while p-Akt immunostaining was increased in groups 3 and 4. The number of IL-1 beta immunostained cells in groups 3 and 4 was decreased compared to group 2. INSL-3 immunostaining was increased significantly in group 3 compared to group 2. Our findings indicate that proanthocyanidin ameliorated diabetes related testicular dysfunction. Proanthocyanidin contributes to a balanced oxidant-antioxidant status, and balanced proliferation and apoptosis activity in the germinal cells.en10.1080/10520295.2021.2002931info:eu-repo/semantics/closedAccessAktIL-1 BetaApoptosis INSL-3Diabetes MellitusJNKProanthocyanidinRatTestisTGF-Beta 1Insulin-Like Factor-3Oxidative StressZinc-DeficiencyDown-RegulationActivationExpressionToxicityFormaldehydeExtractPathwayArticle975363371Q4WOS:0007201751000012-s2.0-8511944191434789048Q2