Effects of Morin on the Wnt, Notch1/Hes1, KI-67/3-Nitrotyrosine and Damage Signaling Pathways in Rats Subjected to Experimental Testicular Ischemia/Reperfusion

Testicular torsion, which occurs when the testicle rotates around the axis of the spermatic cord, is a serious cause of hospital admission, mostly in newborns and children, but also in adults. Oxidative stress is an important mediator of the development of complications. Morin has anti-inflammatory, anti-autophagic, and anti-apoptotic activities and especially strong antioxidant activity. This study aimed to determine the effects of Morin on testicular torsion injury. Methods: 35 Wistar rats were divided into 5 groups (n = 7): Control, Morin, I/R, I/R + MRN50, and I/R + MRN100. Parameters are effective in oxidative stress, inflammation, endoplasmic reticulum stress, apoptosis, and autophagy damage and Wnt pathway parameters, KI-67, and 3-NT levels were analyzed by biochemical, molecular, and histological methods. Results: I/R injury significantly increased oxidative stress (MDA, p < 0.001) and reduced antioxidant activity (GSH, SOD, CAT, GPx; p < 0.001). MRN administration reversed these effects, with higher doses showing greater improvement (p < 0.01 for CAT, p < 0.001 for others). Inflammation markers (NF-kB, IL-1β, TNF-α, COX-2, iNOS) were elevated in the I/R group, but MRN reduced their expression (p < 0.001). MRN also mitigated ER stress and reactivated the Wnt signaling pathway, particularly at 100 mg/kg (p < 0.001). Additionally, MRN reduced apoptosis (Caspase-3, Bax, p < 0.001) and autophagy (Beclin-1, LC3A, LC3B, p < 0.001), and improved testicular histology and sperm parameters. MRN treatment restored sperm density, motility, and viability (p < 0.05), with higher doses proving more effective. Conclusion: MRN has effects properties in testicular I/R injury by inhibiting many damage pathways and activating protective mechanisms.