Abstract
Varicocele (VC) is an abnormal tortuosity and venous distension of the pampiniform plexus in the spermatic cord. VC is the most common surgically correctable cause of male infertility. The purpose of the present study was to investigate the effects of VC on the tight junctions and the blood‑testis barrier (BTB) of Sertoli cells in the bilateral testes of rats. A model of VC was established by left renal vein narrowing in Sprague‑Dawley rats; control rats underwent dissection of the vein without narrowing. The bilateral testes were harvested at 4, 6 and 8 weeks after the operation. The relative expression of claudin‑11 and transforming growth factor (TGF)‑β in the testis was determined by reverse transcription‑polymerase chain reaction analysis and immunohistochemistry (IHC). The expression level of claudin‑11 was prominently downregulated in the VC model group compared with the control group, while the level of TGF‑β in the testes was higher in the VC group. IHC examination demonstrated that VC led to destruction of the integrity of the BTB, and the degree of destruction increased with time. Furthermore, it was also observed that unilateral VC affected contralateral testicular function. In conclusion, the present study partially explained the molecular mechanisms underlying the pathogenesis of VC and provided grounds for further research into the treatment of male infertility.