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Protective effect of minocycline on dexamethasone induced testicular germ cell apoptosis in mice
M Orazizadeh1, M Hashemitabar, L Khorsandi
1Department of Anatomical Sciences, Faculty of Medicine, Ahwaz Jundi-Shapour University of Medical Sciences, Ahwaz, Iran.
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.
Insights
Minocycline protects male fertility by reducing germ cell apoptosis caused by dexamethasone (Dex). This study shows minocycline can be a beneficial medication to safeguard sperm production.
Area of Science:
- Reproductive Biology
- Pharmacology
- Cell Biology
Background:
- Apoptosis contributes to testicular germ cell loss, impacting male fertility.
- Minocycline has demonstrated neuroprotective and antiapoptotic properties in prior research.
Purpose of the Study:
- To investigate the protective effects of minocycline against dexamethasone-induced testicular germ cell apoptosis.
- To evaluate minocycline's potential to mitigate the adverse effects of glucocorticoids on male reproductive health.
Main Methods:
- Male mice were administered minocycline, dexamethasone (Dex), or a combination of both daily for seven days.
- Testicular germ cell apoptosis was assessed using the TUNEL method.
- Spermatogenesis quality (Johnsen score) and sperm counts were evaluated.
Main Results:
- Dexamethasone significantly increased germ cell apoptosis and reduced sperm counts and spermatogenesis quality compared to controls.
- Co-administration of minocycline with dexamethasone inhibited germ cell apoptosis.
- Minocycline treatment significantly improved Johnsen scores and sperm counts in Dex-treated mice.
Conclusions:
- Minocycline demonstrates a protective effect against dexamethasone-induced testicular germ cell apoptosis.
- Minocycline shows potential as a therapeutic agent to preserve male fertility by preventing germ cell loss.