Context: Curcumin is a yellow-orange polyphenol derived from turmeric [Curcuma longa L. (Zingiberaceaerhizomes)]. Turmeric is a main ingredient of Indian, Persian, and Thai dishes. Extensive studies within the last half a century have demonstrated the protective action of curcumin in many disorders of the body.
Objective: This study evaluated the protective effect of curcumin on dexamethasone-induced spermatogenesis defects in mice.
Materials and methods: Thirty-two NMRI mice were randomly divided into 4 groups. The first (control) group received 1 mL/day of distilled water by intraperitoneal (i.p.) injection for 7 days. The second group received 200 mg/kg/day of curcumin (Cur) for 10 days. Third group received 7 mg/kg/day of dexamethasone (Dex) for 7 days. Forth group received 200 mg/kg of curcumin for 10 days after dexamethasone treatment. Testicular histopathology, morphometric analysis, head sperm counting, and immunohistochemistry assessments were performed for evaluation of the dexamethasone and curcumin effects.
Results: Expression of Bcl-2 was significantly increased in the curcumin + dexamethasone group compared with dexamethasone-treated animals (p < 0.05). Dexamethasone induced spermatogenesis defects including epithelial vacuolizations, sloughing of germ cells, reduction of seminiferous tubule diameter, reduction in the number of sperm heads and significant maturation arrest (p < 0.001). Curcumin + dexamethasone treatment significantly prevented these changes (p < 0.05).
Discussion and conclusion: The results of this study demonstrate that curcumin increases the expression of Bcl-2 protein, an important anti-apoptotic factor, and improves the spermatogenesis defects in dexamethasone treated mice. Curcumin has a potent protective effect against the testicular toxicity and might be clinically useful.