Rho-kinase levels in testicular ischemia-reperfusion injury and effects of its inhibitor, Y-27632, on oxidative stress, spermatogenesis, and apoptosis.

OBJECTIVE

To investigate testicular Rho-kinase levels and the effects of its inhibitor, Y-27632, on oxidative stress, spermatogenesis, and apoptosis in testicular ischemia-reperfusion rat model.

METHODS

The study included 29 adult Wistar-Albino male rats weighing 150-200 g. The rats were divided into 3 groups. Group 1 underwent sham operation (n = 10). In group 2, left testicular torsion-detorsion was performed (n = 9). In group 3, Rho-kinase inhibitor Y-27632 (5 mg/kg) was injected intraperitoneally 30 minutes before detorsion (n = 10). Two months later, bilateral orchiectomy was performed in all the groups. Rho-kinase levels by Western blotting, apoptosis with terminal deoxynucleotidyl transferase dUTP nick end labeling method, testicular damage and spermatogenesis with modified Johnsen score, testicular total antioxidative status, and total oxidative status were measured.

RESULTS

In the torsion-detorsion (T/D) group, Rho-kinase level increased significantly, compared with the sham group (P = .025). In the Y-27632 treatment group, Johnsen scores were significantly higher, and apoptosis indexes were significantly lower, compared with the T/D group (P = .001). Significantly higher total antioxidative status levels and lower total oxidative status levels were observed in the Y-27632 treatment group, compared with the T/D group (P = .001 and P = .002, respectively).

CONCLUSION

Testicular ischemia-reperfusion significantly increased Rho-kinase levels in rats, and administration of Rho-kinase inhibitor, Y-27632, before detorsion might prevent ischemia-reperfusion injury.