The antioxidant role of agomelatine and gallic acid on oxidative stress in STZ induced type I diabetic rat testes
Erişim
info:eu-repo/semantics/closedAccessTarih
2017Yazar
Yigitturk, GurkanAcara, Ahmet Cagdas
Erbas, Oytun
Oltulu, Fatih
Yavasoglu, Nefise Ulku Karabay
Uysal, Aysegul
Yavasoglu, Altug
Üst veri
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Diabetes is a multisystem disorder and its effects are observed on the reproductive system. One of the main causes of testicular tissue damage is diabetes-induced overproduction of reactive oxygen species and glycated end products. The main objectives of this study were to investigate the possible effects of agomelatine (AG) and gallic acid (GA) in suppressing oxidative stress in Type I diabetes induced testicular damage. A total of 28 adult male rats were included in the study. Diabetes was induced by intraperitoneal injection of streptozocin (STZ, 55 mg/kg) to 21 rats, which were then randomly assigned to 3 groups; 1 mL saline solution was given to the diabetes + saline group by oral gavage, 20 mg/kg/day oral AG was given to the diabetes + AG group, and 20 mg/kg/day oral GA was given to the diabetes + GA group for 4 weeks. Tumor necrosis factor alpha (TNF alpha), nitric oxide synthase 2 (NOS2), fibronectin and vascular endothelial growth factor (VEGF) were used for the investigation of inflammation, fibrosis and vascular structures. The terminal-deoxynucleoitidyl-transferase mediated nick end-labeling assay (TUNEL) was used to detect apoptosis. Testicular tissue total antioxidant capacity values were tested by biochemical analysis. AG treatment showed an improvement on biochemical parameters and histopathological appearance on the rat testes. GA showed dose-related regenerative effects on biochemical parameters. Histologically, a minimal healing effect was determined on the testes damage. In conclusion, it was observed that AG is a potentially beneficial agent for reducing testicular damage by decreasing oxidative stress level. However, GA was seen to have a poor therapeutic effect. (C) 2016 Elsevier Masson SAS. All rights reserved.