Alireza Samie1, Reza Sedaghat2, Tourandokht Baluchnejadmojarad3, Mehrdad Roghani4. 1. School of Medicine, Shahed University, Tehran, Iran. 2. Department of Anatomy and Pathology, School of Medicine, Shahed University, Tehran, Iran. 3. Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. 4. Neurophysiology Research Center, Department of Physiology, Shahed University, Tehran, Iran. Electronic address: mroghani@shahed.ac.ir.
Abstract
AIM: This study was designed to assess the beneficial effect of hesperetin on diabetes-associated testicular injury in the rat. MAIN METHODS: Oral treatment with hesperetin started 10 days after diabetes induction by streptozotocin (60 mg/kg, i.p.) for 46 days. Testicular damage was evaluated by histological evaluation of seminiferous tubules in addition to assessment of epididymal sperm count, motility, and viability. In addition, testicular biomarkers of apoptosis, inflammation, and oxidative stress were also determined. KEY FINDINGS: Hesperetin treatment of diabetic group prevented body weight loss and reduced serum glucose in addition to improvement of serum testosterone. Additionally, hesperetin-treated diabetic group had lower levels of malondialdehyde (MDA), reactive oxygen species (ROS), protein carbonyl, DNA fragmentation, and caspase 3 activity as specific biomarkers of oxidative stress and/or apoptosis. Furthermore, hesperetin augmented testicular antioxidant system as shown by higher levels of glutathione (GSH), mitochondrial membrane potential (MMP), and ferric reducing antioxidant power (FRAP) in addition to improvement of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx). Moreover, hesperetin administration to diabetic rats attenuated testicular indices of inflammation consisting of tumor necrosis factor α (TNFα) and interleukin 17 (IL-17) and prevented damage of seminiferous tubules as revealed by higher levels of sperm count, motility, and viability in diabetic rats. SIGNIFICANCE: Collectively, hesperetin could alleviate testicular damage in DM, at least through inhibition of apoptosis, oxidative stress, and inflammation in addition to its up-regulation of endogenous enzymatic and non-enzymatic antioxidants.
AIM: This study was designed to assess the beneficial effect of hesperetin on diabetes-associated testicular injury in the rat. MAIN METHODS: Oral treatment with hesperetin started 10 days after diabetes induction by streptozotocin (60 mg/kg, i.p.) for 46 days. Testicular damage was evaluated by histological evaluation of seminiferous tubules in addition to assessment of epididymal sperm count, motility, and viability. In addition, testicular biomarkers of apoptosis, inflammation, and oxidative stress were also determined. KEY FINDINGS:Hesperetin treatment of diabetic group prevented body weight loss and reduced serum glucose in addition to improvement of serum testosterone. Additionally, hesperetin-treated diabetic group had lower levels of malondialdehyde (MDA), reactive oxygen species (ROS), protein carbonyl, DNA fragmentation, and caspase 3 activity as specific biomarkers of oxidative stress and/or apoptosis. Furthermore, hesperetin augmented testicular antioxidant system as shown by higher levels of glutathione (GSH), mitochondrial membrane potential (MMP), and ferric reducing antioxidant power (FRAP) in addition to improvement of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx). Moreover, hesperetin administration to diabeticrats attenuated testicular indices of inflammation consisting of tumor necrosis factor α (TNFα) and interleukin 17 (IL-17) and prevented damage of seminiferous tubules as revealed by higher levels of sperm count, motility, and viability in diabeticrats. SIGNIFICANCE: Collectively, hesperetin could alleviate testicular damage in DM, at least through inhibition of apoptosis, oxidative stress, and inflammation in addition to its up-regulation of endogenous enzymatic and non-enzymatic antioxidants.