Celecoxib and silymarin attenuated varicocele-induced damages at testicular and sperm levels; evidence for endocrine and antioxidant statuses

Mazhari, S.; Razi, M.; Malekinejad, H.; Sadrkhanlou, R.
June 2014
Iranian Journal of Reproductive Medicine;Jun2014 Supplement, Vol. 12, p117
Academic Journal
Introduction: Varicocele (VCL) results in considerable disorders in male reproductive potential. Varicocele exerts its impact via enhancing infiammation and downregulating testicular endocrine and antioxidant statuses. Celecoxib (CCB) is a non-steroidal anti-infiammatory drug (NSAID), which is used as cyclooxygenase-2 (COX-2) inhibitor. Silymarin (SMN) is a fiavonoid complex, which is known for its antioxidant potenfial. Present study was designed for evaluating the protective effect of CCB and SMN on VCL-induced damages in testicles and sperm cells. Materials and Methods: VCL was induced in 24 mature male rats and then animals were randomly divided into four groups including; non-treated VCL induced, CCB-treated (10mg/kg, orally), SMN-treated (100mg/kg, orally), SMN+CCB-treated groups. Following 60 days after VCL induction, spermatogenesis ratio evaluated by assessing tubular differentiation (TDI), repopulation (RI) indexes. Leydig cells steroid foci were evaluated by using epifiuorescent staining. Immune eels infiltration, tissue total antioxidant capacity (TAC) and malondialdehyde (MDA) content as well as sperm count, motility, abnormality and DNA damage were analyzed. Results: CCB and SMN co-administration elevated VCL-reduced TDI, RI and SPI and reduced immune cells infiltrafion. The Leydig cells steroidogenic foci increased in CCB+SMN, SMN and CCB-treated groups, respecfively. SMN+CCB significantly (p<0.05) upregulated VCL-reduced TAC and reduced tissue MDA. All treated animals exhibited remarkably (p<0.05) higher sperm count, sperm motility, viability and reduced sperm abnormality and DNA damage. However it was more pronounced in SMN+CCB-treated group. Conclusion: Our data suggest that, SMN inhibited the VCL-induced damages via up-regulating antioxidant status and CCB limited the disorders by attenuating VCL-induced inflammation.


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