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

Author(s): Orazizadeh M, Hashemitabar M, Khorsandi L

Affiliation(s): Department of Anatomical Sciences, Faculty of Medicine, Ahwaz Jundi-Shapour University of Medical Sciences, Ahwaz, Iran.

Publication date & source: 2009-01, Eur Rev Med Pharmacol Sci., 13(1):1-5.

Publication type: Research Support, Non-U.S. Gov't

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.