Effect of sunitinib on testicular oxidative and proinflammatory damage induced by ischemia–reperfusion in rats

Abstract

Introduction

This study aimed to biochemically and histopathologically investigate the effect of sunitinib on oxidative testicular damage induced by ischemia/reperfusion in rats.

Material-method

Experimental animals were divided into three groups of six rats each: testicular torsion–detorsion (TTD), sunitinib + testicular torsion–detorsion (STD), and sham control (SC). Sunitinib (25 mg/kg) was administered orally to the STD group by gavage. Normal saline (0.9% NaCl) was administered orally to the TTD and control groups as the solvent. One hour after administration of sunitinib and 0.9% NaCl, all animal groups were done torsion–detorsion. Then, all the rats were killed by high-dose anesthesia, and their testicles were removed. Biochemical and histopathological examinations were performed on the removed testicular tissues.

Results

Malondialdehyde; it was observed that the results in the STD group were close to those of the SC group and statistically significant lower compared to the TTD group (p = 0.001). The glutathione values were statistically significantly higher in the STD group compared to the TTD group (p < 0.001). Nuclear factor kappa B values, revealing a statistically significant difference between the TTD and STD groups (p < 0.001). The TNF-α levels were measured and indicating that the results of the STD group were statistically significantly lower than those of the TTD group (p < 0.001). Histopathologically, animal tissues given sunitinib were observed to resemble normal tissues.

Conclusion

Sunitinib was shown to prevent histopathological changes in testicular tissue against ischemia/reperfusion damage.