The effects of Dexamethasone on Galectin-3 expression in the mouse testicular tissue

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. 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. Res ults: 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) Reduction in expression of Gal-3 in seminiferous tubules in Dex treated mice indicates that it probably involves in testicular germ cell apoptosis.