Protective effects of quercetin against apoptosis and oxidative stress in streptozotocin-induced diabetic rat testis

The aim of this study was to investigate the protective effect of quercetin (QE) on oxidative stress, apoptosis, and cell proliferation in the rat testis after streptozotocin (STZ)-induced diabetes. Diabetes was induced by a single intraperitoneal injection of STZ (50 mg/kg). The rats in the QE-treated group were given QE (15 mg/kg) once a day intraperitoneally for 8 weeks starting 3 days prior to STZ injection. At the end of the study, all animals were sacrificed. Testis tissues and blood samples were collected for histopathologic and biochemical analysis. QE treatment significantly decreased the elevated tissue malondialdehyde (MDA) levels and increased the reduced superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) enzyme activities in testis tissues samples. The QE-treated rats in the diabetic group showed an improved histologic appearance and serum testosterone levels. Our data indicate a significant reduction in the activity of in situ identification of apoptosis using terminal dUTP nick end-labeling (TUNEL) and there was a rise in the expression of proliferating cell nuclear antigen (PCNA) in testis tissues of QE-treated rats in the diabetic group. These results suggest that administration of QE is a potentially beneficial agent to reduce testicular damage in diabetic rats by decreasing oxidative stress.

► QE treatment significantly decreased the elevated tissue MDA levels. ► QE treatment significantly increased of reduced SOD and GSH-Px enzyme activities. ► Treatment with QE reduced the reactivity and the number of germ cell apoptosis. ► The PCNA index was significantly increased in the diabetic treated with QE group.