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Dexamethasone effects on Bax expression in the mouse testicular germ cells
Hashemitabar Mahmoud1, Orazizadeh Mahmoud, Khorsandi Layasadat
1Department of Anatomical Sciences, Faculty of Medicine, Ahvaz Jundi-Shapour University of Medical Sciences, Ahwaz - Iran.
Abstract:
Exposure to glucocorticoids (GCs) leads to numerous changes in various biological systems including the reproductive system. The aim of the present study was to find out whether dexamethasone (Dex), a widely used GC, would influence the apoptosis and expression of Bax, an important proapoptotic protein, in the mouse testicular germ cells. Experimental groups of 8 male NMRI mice received one of the following treatments daily for 7 days: 4, 7 and 10 mg/kg Dex. Control groups were treated with equivalent volumes of saline. Experimental and control animals were sacrificed 24 h after the last injection. Immunohistochemical procedure was used to evaluation of Bax expression and the deoxyuridine nick-end labeling (TUNEL) was applied to assessment of the apoptotic germ cells. Bax expression was upregulated mainly at stages VII-VIII of spermatogenic cycle (p<0.05) in experimental groups. Apoptotic index was significantly increased in 7 and 10 mg/kg Dex treated mice (p<0.05). It appears that GCs such as Dex could induce apoptosis through the expression of proapoptotic proteins.
Insights
Glucocorticoids (GCs), like dexamethasone (Dex), increase apoptosis in mouse testicular germ cells. Dex also upregulates Bax, a proapoptotic protein, suggesting GCs can induce germ cell death.
Area of Science:
- Reproductive biology
- Endocrinology
- Cell biology
Background:
- Glucocorticoids (GCs) impact multiple biological systems, including reproduction.
- Understanding GC effects on testicular germ cells is crucial for reproductive health.
Purpose of the Study:
- To investigate the influence of dexamethasone (Dex), a synthetic GC, on apoptosis.
- To examine the expression of the proapoptotic protein Bax in mouse testicular germ cells following Dex exposure.
Main Methods:
- Male NMRI mice were administered daily doses of 4, 7, or 10 mg/kg Dex for 7 days.
- Control groups received saline injections.
- Bax expression was evaluated using immunohistochemistry.
- Apoptosis was assessed via the TUNEL assay.
Main Results:
- Dexamethasone significantly upregulated Bax expression, particularly at stages VII-VIII of spermatogenesis (p<0.05).
- A significant increase in the apoptotic index was observed in mice treated with 7 and 10 mg/kg Dex (p<0.05).
Conclusions:
- Dexamethasone exposure induces apoptosis in mouse testicular germ cells.
- GCs, exemplified by Dex, may trigger germ cell apoptosis through the upregulation of proapoptotic proteins like Bax.
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