Yigitturk Gurkan, Acara Ahmet Cagdas, Erbas Oytun, Oltulu Fatih, Yavasoglu Nefise Ulku Karabay, Uysal Aysegul, Yavasoglu Altug
Ege University, Faculty of Medicine, Department of Histology and Embryology, Izmir, Turkey.
Gaziemir State Hospital, Department of Emergency Medicine, Izmir, Turkey.
Biomed Pharmacother. 2017 Mar;87:240-246. doi: 10.1016/j.biopha.2016.12.102. Epub 2017 Jan 3.
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, 55mg/kg) to 21 rats, which were then randomly assigned to 3 groups; 1mL saline solution was given to the diabetes+saline group by oral gavage, 20mg/kg/day oral AG was given to the diabetes+AG group, and 20mg/kg/day oral GA was given to the diabetes+GA group for 4 weeks. Tumor necrosis factor α (TNFα), 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.
糖尿病是一种多系统疾病,其对生殖系统会产生影响。睾丸组织损伤的主要原因之一是糖尿病诱导的活性氧和糖基化终产物过度产生。本研究的主要目的是探讨阿戈美拉汀(AG)和没食子酸(GA)对抑制1型糖尿病诱导的睾丸损伤中氧化应激的可能作用。该研究共纳入28只成年雄性大鼠。通过腹腔注射链脲佐菌素(STZ,55mg/kg)诱导21只大鼠患糖尿病,然后将其随机分为3组;糖尿病+生理盐水组经口灌胃给予1mL生理盐水,糖尿病+AG组经口给予20mg/kg/天的AG,糖尿病+GA组经口给予20mg/kg/天的GA,持续4周。使用肿瘤坏死因子α(TNFα)、一氧化氮合酶2(NOS2)、纤连蛋白和血管内皮生长因子(VEGF)来研究炎症、纤维化和血管结构。采用末端脱氧核苷酸转移酶介导的缺口末端标记法(TUNEL)检测细胞凋亡。通过生化分析检测睾丸组织的总抗氧化能力值。AG治疗对大鼠睾丸的生化参数和组织病理学外观有改善作用。GA对生化参数显示出剂量相关的再生作用。组织学上,确定对睾丸损伤有最小的愈合作用。总之,观察到AG是一种通过降低氧化应激水平来减少睾丸损伤的潜在有益药物。然而,GA的治疗效果不佳。