Naringin attenuates testicular ischemia/reperfusion injury in a mouse torsion/detorsion model via intraperitoneal administration.

Abstract

This study investigated the protective effects of naringin, a flavanone glycoside with established antioxidant, anti-inflammatory, and anti-apoptotic properties, against testicular ischemia/reperfusion (I/R) injury in a mouse torsion/detorsion model. Forty adult male mice underwent a 720° torsion for two hours, followed by detorsion. Five groups (n = 8) received naringin (50, 100, or 200 mg/kg) administered intraperitoneally 30 min prior to detorsion: sham, T/D, and three T/D + naringin groups. After 30 days, sperm quality (concentration, motility, kinematics), oxidative stress markers, histological alterations, apoptotic markers (Bcl-2, Bax, caspase-3), hormonal profiles, and fertility outcomes were evaluated. The T/D group exhibited deteriorated sperm quality, reduced antioxidant levels (TAC, SOD, GPx), decreased hormones (testosterone, FSH, LH), elevated MDA and apoptotic markers, and impaired fertility. Notably, FSH levels decreased after T/D - in contrast to the typical increase in chronic damage models - possibly due to acute-phase pituitary suppression in this short-term mouse model. Naringin (particularly 100 and 200 mg/kg) dose-dependently improved sperm parameters, antioxidant status, testicular histology, hormonal levels, and fertility. The 50 mg/kg dose showed limited efficacy. Naringin inhibited apoptosis by upregulating Bcl-2 and downregulating Bax and caspase-3. These results indicate that intraperitoneal naringin, especially at 100-200 mg/kg, exerts significant protective effects against testicular I/R injury and may warrant further investigation as a potential adjunctive therapy in the clinical management of testicular torsion.