Background : Previous studies have demonstrated that Dexamethasone, a widely used GC, induces apoptosis in testis by decreasing the testosterone levels. Galectin-3 (Gal-3), a member of the ß-galactoside-binding lectins, plays critical roles in diverse biological events including cell growth, apoptosis, cell adhesion and immunomodulation. In this study, the effects of Dexamethasone (Dex) on galectin-3 (Gal-3) expression in the mouse testicular tissue were investigated. Materials and Methods: Sixteen male NMRI (6-8 weeks old) randomly divided into two groups. Experimental group received 7 mg/kg Dex for 7 days by intrapritoneal injection. Control group received normal saline for 7 days by intrapritoneal injection.One day after the last injection the mice were sacrificed and the samples were collected (from adult NMRI mice), fixed in 10% buffered formalin and embedded in paraffin for immunohistochemistry and TUNEL studies. HSCORE was used for scaling and comparison of results. Res‌ults: In the control group, seminiferous tubules showed positive immunoreactivity to Gal-3 at all stages. In particular, stages of VII-VIII showed the most immunoreactivity. The expression pattern of Bcl-2 and Galectin-3 was similar in both control and experimental groups. HSCORE assessments showed a significant decrease in expression of Gal-3 at all stages of spermatogenic cycle in Dex treated mice (P<0.001). ). Apoptotic index (AI) showed a significant increase at all stages of spermatogenesis cycle in the experimental group (P<0.01) Conclusion: Reduction in expression of Gal-3 in seminiferous tubules in Dex treated mice indicates that it probably involves in testicular germ cell apoptosis.

Keywords: Dexamethasone, Galectin-3, Apoptosis, Testis

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