Testicular torsion is a common urological emergency, and delayed treatment often leads to testicular ischemic necrosis. Its incidence presents two peak periods, namely infancy and adolescence. Unilateral testicular torsion severely impairs the function of the affected testis and also causes secondary damage to the contralateral testis. Postoperatively, it frequently results in reduced spermatogenic capacity and altered hormone secretion, ultimately inducing male infertility. Clinically, the severity of testicular injury caused by acute spermatic cord torsion is positively correlated with the torsion degree and ischemic duration. Even with timely reduction, testicular torsion can still trigger testicular ischemia‑reperfusion injury, leading to biochemical and morphological abnormalities in testicular tissues. Accordingly, therapeutic intervention following testicular torsion reduction has become a crucial research topic.

SD rats (male, 200–300 g)
Modeling method: The testis and epididymis were dissociated, and the gubernaculum testis was ligated and transected. The isolated testis was rotated clockwise twice along its long axis and maintained for 2 hours to establish the testicular ischemia-reperfusion model.
Evaluation index: HE staining

Testicular HE staining