Related Experiment Video
Updated: Jun 20, 2026
Bilateral Common Carotid Artery Occlusion as an Adequate Preconditioning Stimulus to Induce Early Ischemic Tolerance to Focal Cerebral Ischemia
Published on: May 9, 2013
Ischemic preconditioning and post-conditioning to decrease testicular torsion-detorsion injury
Shogo Shimizu1, Motoaki Saito, Yukako Kinoshita
1Division of Molecular Pharmacology, Department of Pathophysiological and Therapeutic Science, Tottori University Faculty of Medicine, Yonago City, Tottori, Japan.
Purpose:
The main pathophysiology of torsion-detorsion is associated with ischemia-reperfusion injury in the testis caused by the twisted spermatic cord and its release. It is most likely mediated by oxygen free radicals. We investigated the effects of ischemic preconditioning and post-conditioning on rat testicular ischemia-reperfusion injury.
Materials And Methods:
Eight-week-old male Sprague-Dawley rats (SLC, Shizuoka, Japan) were randomly divided into 4 age matched groups, including 1-control sham operation, 2-60-minute ischemia/120-minute reperfusion, 3-3 cycles of 5-minute ischemia/5-minute reperfusion and then 60-minute ischemia/120-minute reperfusion (ischemic preconditioning) and 4-60-minute ischemia, 5 cycles of 10-second reperfusion/10-second ischemia and then 120-minute reperfusion (ischemic post-conditioning). After sacrifice the levels of malondialdehyde, 8-hydroxydeoxyguanosine, myeloperoxidase, superoxide dismutase, catalase, heat shock protein 70 protein and mRNA, and DNA fragmentation were measured in the rat testes. Testicular tissue was also histologically analyzed.
Results:
The levels of malondialdehyde, 8-hydroxydeoxyguanosine, myeloperoxidase, heat shock protein 70 mRNA, superoxide dismutase, catalase, DNA fragmentation and apoptosis cells were significantly higher in the ischemia-reperfusion group than in controls. Ischemic preconditioning decreased histological parameters, including vacuolation and necrosis, and decreased malondialdehyde, 8-hydroxydeoxyguanosine, myeloperoxidase, heat shock protein 70 mRNA but not protein, superoxide dismutase, catalase, DNA fragmentation and apoptosis compared to the ischemia-reperfusion group. Ischemic post-conditioning ameliorated 8-hydroxydeoxyguanosine, superoxide dismutase, heat shock protein 70 mRNA, DNA fragmentation and apoptosis compared to the ischemia-reperfusion group.
Conclusions:
Our data indicate that ischemic preconditioning and post-conditioning ameliorated the testicular damage induced by ischemia-reperfusion injury.
