Effect of dexpanthenol on cyclophosphamide-induced ovarian toxicity: a histological and molecular study in rats

Research question Does the administration of Dexpanthenol (Dex) an effective therapeutic agent against Cyclophosphamide (CYC)-induced premature ovarian failure (POF) in rats? Design A total of 28 female Wistar Albino rats were randomly divided into four groups (n=7/group). The POF and POF + Dex groups were intraperitoneally administered CYC at an initial dose of 50 mg/kg, followed by 8 mg/kg for 14 days. The Dex and POF + Dex groups were both intraperitoneally administered Dex at a dose of 500 mg/kg/day for 15 days. Results In the group administered CYC, a decrease was observed in the ovarian index, the numbers of primordial, primary, secondary, and antral follicles; an increase in the number of corpus luteum and atretic follicles; a decrease in PCNA immunoreactivity; a significant reduction in AMH and E2 levels, along with an increase in serum FSH levels. Dex, on the other hand, reversed these effects. qRT-PCR analyses showed that Dex increased Bcl-2, Akt1, mTOR, Nrf2, and HO-1 in CYC-induced ovarian tissues. Also, Dex decreased Bax, Cas3, Hsp27, Hsp70, and Hsp90 in tissues. Dex treatment inhibited the intrinsic apoptotic pathway and oxidative stress levels in ovarian tissues via the down-regulation of heat shock proteins and the activation of Nrf2/HO-1 pathways. Conclusions Our findings demonstrated that Dex is an effective agent against POF caused by CYC, yet further experimental and clinical data are needed to use it effectively.