P-31: Dexamethasone and Vitamin E Up-Regulated The Varicocele-Reduced Hsp70 Protein Expression; Correlation with Testicular Tissue Inflammation and Antioxidant Status

Background: The varicocele (VCL) impacts the testicular tissue both by enhancing tissue inflammation and by down-regulating the antioxidant status. On the other hand, in varicocele patient the critical role of Hsp70 in spermiogenesis is identified. Therefore present study was estimated to evaluate the protective effect of testosterone and vitamin E on VCL-decreased Hsp70 expression and on VCL-induced inflammation. Materials and Methods: Thirty mature male rats were divided into five control-sham and test groups (N=6 rats for each group). The test groups underwent to an experimental varicocele as Group VCL alone (varicoceleinduced, for 60 days), group VCL+Dexamethasone (45μg intraperitoneally, for 60 days), group VCL+vitamin E (150mg/kg, orally, for 60 days) and group VCL+dexamethasone+vitamin E. The Western blotting and immunohistochemical analyses for Hsp70 protein were performed. The total RNA, total protein, tissue alkaline phosphatase ALP and acid phosphatase (ACP) levels were evaluated. The Epi-fluorescent and fluorescent analyses were conducted to evaluate the germinal cells RNA damage and leydig cells biosteroid activity, respectively. Results: The VCL+dexamethasone+vitamin E group showed the highest level of Hsp70 protein beside higher detected immunohistochemical spots in germinal cells. The animals in all treated groups showed remarkably (p<0.05) higher total protein and normal RNA contents versus VCL alone group. The higher biosteroidogenesis was observed in vitamin E and dexamethasonerecieved groups leydig cells. Dexamethasone-received animals showed the lowest levels of ALP and ACP versus other groups. Conclusion: Our data showed that dexamethasone by inhibiting inflammation and the vitamin E by up-regulating testicular antioxidant capacity could inhibit the VCLinduced damages.