褪黑素通过抑制铁死亡改善环磷酰胺和白消安诱导的早发性卵巢功能不全小鼠的研究OA

Objective To investigate the protective effect and mechanism of melatonin on cyclophosphamide and busulfan-induced premature ovarian insufficiency(POI)in mice by inhibiting ferroptosis pathway.Methods 6-week-old CD1 female mice were randomly divided into the control group,the POI group,and the POI+melatonin group.After establishing the POI model,mouse body weight,ovarian wet weight,serum hormone levels,follicle count,and ferroptosis related indices were detected.Results The weight,follicle count,and hormone levels of the POI group mice were significantly lower than those of the control group(P＜0.05),and the ferroptosis markers malondialdehyde,nuclear transcription factor E2 related factor,recombinant solute carrier family 7,member 11,and glutathione peroxidase 4 all increased(P＜0.01).After melatonin intervention,the body weight,follicle count,and serum hormone levels of mice all significantly improved(P＜0.05),while the expression levels of ferroptosis related markers malondialdehyde,glutathione,and nuclear transcription factor E2 related factor were significantly reduced(P＜0.01).Conclusion Melatonin improves POI by inhibiting the ferroptosis pathway and has potential clinical application value.