期刊
ANDROLOGY
卷 10, 期 5, 页码 973-983出版社
WILEY
DOI: 10.1111/andr.13184
关键词
remote ischemic postconditioning; RISK; SAFE; testis; torsion; detorsion
类别
资金
- Sichuan UniversityWest China Hospital
The study found that remote ischemic postconditioning has a protective effect against testicular torsion/detorsion, reducing testicular swelling, preserving morphological integrity and spermatogenesis, and inhibiting testicular apoptosis.
Background Testicular torsion/detorsion can lead to severe testicular damage. The organ-protective effect of remote ischemic postconditioning (RLIPost) against ischemia/reperfusion injury has been characterized; however, it remains unknown whether RLIPost has a testicular protective effect. Objectives Here, we tested the hypothesis that RLIPost can protect the testes in a rat model of testicular torsion/detorsion in vivo. Materials and methods Male Sprague-Dawley rats were assigned to sham-operated, control, or remote liver and limb ischemic postconditioning-treated groups. Testicular torsion/detorsion was performed by 3 h of testicular torsion (720 degrees clockwise unilateral spermatic cord torsion), followed by 3 h of detorsion. For liver and limb ischemic postconditioning, four cycles of 5 min of liver or limb ischemia with 5-min intermittent reperfusion stimuli were conducted at the onset of testicular reperfusion. Results Liver and limb ischemic postconditioning significantly ameliorated ipsilateral and contralateral testicular swelling responses, preserved morphological integrity and spermatogenesis and inhibited testicular apoptosis. In addition, RLIPost enhanced the phosphorylation of AKT/ERK1/2/GSK-3 beta/STAT-3 in the ipsilateral testis while suppressing JNK activation in the ipsilateral and contralateral testes. Discussion and conclusion To the best of our knowledge, this study is the first to demonstrate the involvement of RLIPost in an animal model of testicular torsion/detorsion. We showed that RLIPost protects both ipsilateral and contralateral testes against testicular torsion/detorsion in vivo, via at least in part, the RISK and SAFE-mediated signaling pathways.
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