Protective effect of minocycline on dexamethasone induced testicular germ cell apoptosis in mice.

BACKGROUND Apoptosis involves in testicular germ cell loss in animals and humans, and plays an important role in male fertility. Previous studies have reported neuroprotective and antiapoptotic effects of minocycline. AIM In this study the protective effect of Minocycline on testicular germ cell apoptosis arising from dexamethasone (Dex) has been evaluated. Dex is a widely used as a glucocorticoid (GC) agent that its apoptotic effect has been shown. MATERIALS AND METHODS Experimental groups of 8 male mice received one of the following treatments daily for 7 days: 100 mg/kg Minocycline, 7 mg/kg Dex and 7 mg/kg Dex +100 mg/kg Minocycline. Control group was treated with 0.5 ml saline given orally for a week. Then the mice were sacrificed, and their testes processed for assessment of germ cell apoptosis (TUNEL method), the quality of spermatogenesis (Johnsen score system) and testicular sperm counts. RESULTS Germ cell apoptosis were significantly increased in Dex treated mice compared with control (P < 0.01). Spermatogenesis and the number of sperms head were significantly reduced in Dex treated mice compared with those of the control group (P < 0.01). Treatment with Dex and Minocycline resulted in an inhibition effect on germ cell apoptosis and a significant increase in the Johnsen score and the number of head sperm compared with Dex treated mice (P < 0.05). CONCLUSION The application of Minocycline may serve as a beneficial medication to protect germ cells against apoptosis.