ObjectiveTo explore the effects of ischemic preconditioning on the level of serum testosterone (T) and apoptosis of spermatogenic cells in rabbits with testicular ischemia-reperfusion injury induced by testicular torsion.

METHODSA total of 15 New Zealand male rabbits were randomly divided into groups A (control), B (ischemia-reperfusion), and C (ischemic preconditioning). The animals of group A were subjected to exposure of the right spermatic cord without ischemia, those of group B received 60-minute non-invasive occlusion of the right spermatic cord followed by 3 days of reperfusion, and those of group C underwent 5-minute occlusion plus 5-minute reperfusion of the right spermatic cord followed by the same procedure as that for group B. Then the rabbits were narcotized with 3% barbital sodium, the whole blood collected for examination of the serum T content and the testis tissues obtained from both the ischemic and healthy sides for HE and TUNEL staining.

RESULTSAfter operation, the body weight was significantly increased as compared with the baseline in groups A (［2.65±0.07］ vs ［2.45±0.07］ kg, P<0.05) and C (［3.03±0.11］ vs ［2.92±0.07］ kg, P<0.05), but not in group B (［3.05±0.07］ vs ［3.05±0.07］ kg, P>0.05). The serum T level showed no statistically significant difference in group A before and after operation (［139.59±9.39］ vs ［140.19±9.47］ ng/L, P>0.05), but was remarkably lower after operation than the baseline in groups B ［148.06±3.31］ vs ［74.12±4.00］ ng/L, P<0.01) and C (［133.75±6.48］ vs［94.76±3.13］ ng/L, P<0.01) as well as than the postoperative index in group A (P<0.01). In comparison with group A and the healthy side of group B, the testis tissue of the ischemic side in group B exhibited structural damage of most of the seminiferous tubules with disappearance of spermatogenic cell structures, apoptosis of spermatogenic cells, and exudation of light-eosin edema fluid in the mesenchyme and lumen, with a markedly increased apoptosis index (P<0.01) and a significantly decreased Johsen's score (P<0.01). Compared with ischemic side of group B, The testis tissue of the ischemic side in group C was restored to normal as compared with that in group B, with a dramatically decreased apoptosis index (P<0.01) and a remarkably increased Johnsen's score (P<0.01).

CONCLUSIONSIschemic preconditioning can raise the decreased serum T level and reduce the apoptosis of spermatogenic cells in rabbits with testicular ischemia-reperfusion injury, which could be applied as a potential option for the clinical treatment of testicular ischemia-reperfusion injury.