Combined Effects of Chrysin Supplementation and Exercise Training on Diabetes-Induced Oxidative Stress and Apoptosis in Rat Testicular Tissue

Background: Diabetes mellitus (DM), one of the most pervasive and enduring metabolic diseases, has been demonstrated to adversely impact male fertility. Conversely, both exercise training and Chrysin have been identified as potential interventions capable of mitigating the deleterious effects of diabetes on spermatogenesis. Thus, the current study aims to explore the individual and combined influences of Chrysin supplementation and running exercise on oxidative stress and germ cell apoptosis in the testicular tissue of diabetic adult rats. Materials and Methods: In this experimental study, the DM was induced by streptozotocin (STZ,50 mg/kg). Rats were divided into control (received STZ solvent), DM-sole, Chrysin-sole (50 mg/kg, daily), moderate-intensity running exercise training (MIRET-sole, warm-up, 5 minutes at 30% of Smax1 (Maximum speed); Moderate intensity exercise, 60 minutes at 60% of Smax1, and recovery, 5 minutes to 30% of Smax1), DM+Chrysin, DM+MIRET, and DM+MIRET+Chrysin. Following 8 weeks, the histopathological changes (Johnson's score, epithelial height, and tubular diameter), testicular malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPX), and the mRNA levels of anti-apoptotic gene Bcl-2 and pro-apoptotic gene Bax was analyzed. Results: Chrysin solely and simultaneous with MIRET could remarkably (P=0.001) improve the DM-induced histopathological damages, increase the testicular SOD and GPx levels, and decline the DM-increased MDA content. Moreover, our results showed that Chrysin solely and more simultaneously with MIRET could significantly (P=0.001) decrease the mRNA expression of Bax and improve the Bcl-2 expression and rebalance the Bax/Bcl-2 balance. Conclusion: Our findings showed that co-administration of Chrysin along with MIRET can significantly ameliorate the DM-induced histopathological, and biochemical impairments and reduce the pro-apoptotic impact of DM on testicular tissue.