Vitamin D supplementation stimulates germ cell proliferation in a restraint-stressed mouse.

Restraint stress in the rodent model has been used for anxiety, depression, alongside testicular dysfunction. Vitamin D regulates testicular function, but its effect on restraint stress-related testicular impairment has not been investigated yet. Therefore, the present study has investigated the effects of vitamin D on the testicular function in restraint-stressed mice. The results showed that vitamin D has improved the sperm parameters and testicular architecture. Moreover, testicular architecture showed better protection in the lower dose, along with decreased oxidative stress. Elevated apoptosis in the lower dose of vitamin D-treated mice could be a disposal mechanism for damaged germ cells. The markers of proliferation (GCNA) were elevated in both doses of vitamin D-treated groups, which showed that vitamin D stimulates germ cell proliferation, thereby improving the testicular architecture. However, PCNA expression did not change, and this could be involved in the DNA repair mechanism. The expression of NF-κB was elevated in all the stressed groups, irrespective of vitamin D treatment. Since NF-κB has pro- and anti-apoptotic effects in the testis, thus, its exact role with respect to apoptosis is not known in the present study. We examined the levels of the Vitamin D Receptor (VDR) in the testis. Our findings indicated that VDR expression was reduced in the restraint-stressed group. In conclusion, vitamin D could improve testicular function in the stressed condition by stimulating germ cell proliferation and due to proliferation, the apoptosis could have also been modulated.