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Background: Premature ovarian insufficiency (POI) affects reproductive capacity and endocrine function in women of reproductive age. Preclinical models that reliably recapitulate POI are needed to evaluate ovarian-protective strategies. Methods: Female C57BL/6 mice received a single intraperitoneal injection of cyclophosphamide (120 mg/kg) plus busulfan (30 mg/kg). A subset received an additional cyclophosphamide booster (60 mg/kg) at week 4. Body weight, serum estradiol-2 (E2), and ovarian index (ovary weight compared to control ovary) were assessed weekly for six weeks. Follicle counts were performed on H&E-stained ovarian sections at weeks 1 through 6. Results: Animals experienced a transient ~ 5% body-weight loss in week 1 with full recovery by week 2 (p > 0.05 vs. controls). Ovarian index declined by ~ 50% in the single-injection group by week 4 and remained stable through week 6 (p < 0.05). The booster group exhibited a comparable reduction by week 4 that persisted at weeks 5 and 6 (p > 0.05), indicating maintenance, but no further exacerbation, of ovarian atrophy. Serum E2 dropped by 40% at week 6 in single-injection mice, whereas booster-injected mice showed a 74% decline by week 5 (p < 0.05). Histologically, follicle counts decreased by 84% in the single-injection group (not significant) and by 100% in the booster group by week 6 (p < 0.05). Conclusions: A single dose of cyclophosphamide and busulfan induces sustained ovarian atrophy characteristic of premature ovarian insufficiency (POI), and a delayed booster accelerates hormonal decline without further mass loss. This model offers a standardized platform for testing interventions to preserve ovarian function.