Reproduction, fertility, and development · 2025
Genistein mitigates ovarian dysfunction in a PCOS mouse model by regulating steroidogenesis, apoptosis, and PARP-1 signaling.
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Wang Jin, Lu Fenglan, Guo Zhuoqian, Meng Qiuxian, Gou Tingting, Li Wenkai, Wan Xiaojuan, Akhta Muhammad Faheem, Azzam Mahmoud M, Wu Guoyun
Аннотация
CONTEXT: Polycystic ovary syndrome (PCOS) is a common endocrine disorder marked by hormonal and clinical imbalances. Genistein (GEN), a soy isoflavone with antioxidant properties, has shown promise in PCOS treatment, although its mechanisms remain unclear.
AIMS: This study aimed to investigate the effects of genistein on ovarian dysfunction in a letrozole-induced PCOS mouse model, focusing on steroidogenesis, apoptosis, and PARP-1 signaling.
METHODS: PCOS was induced by oral administration of letrozole (37.5 mg/kg.day) for 21 days. Mice were then divided into the following three groups (n = 10 each) for another 21-day treatment: control (corn oil), PCOS (continued letrozole), and PCOS + GEN (letrozole + genistein, 50 mg/kg.day, i.p.).
KEY RESULTS: Genistein restored estrous cyclicity in 80% of treated mice versus 0% in the PCOS group (P < 0.05). Histologically, it improved follicular morphology, increased granulosa cell thickness and density, and promoted corpora lutea formation. Genistein significantly reduced serum T and P4 concentrations (P < 0.05) and modulated expression of steroidogenic proteins (CYP11A1, CYP19A1, STAR). It also decreased cleaved Caspase-3 and cleaved PARP-1 expression (P < 0.05), and suppressed abnormal PARylation without affecting total PARP-1 expression levels.
CONCLUSIONS: Genistein alleviates ovarian dysfunction in PCOS mice by restoring estrous cyclicity, enhancing follicular development, and normalizing hormone concentrations, through regulation of steroidogenic proteins, inhibition of apoptosis, and modulation of PARP-1 activity.
IMPLICATIONS: These findings support genistein as a potential therapeutic agent for PCOS, targeting the PARP-1-pADPr axis and apoptosis. Further studies are needed to explore upstream mechanisms and evaluate its long-term effects on reproductive health.
AIMS: This study aimed to investigate the effects of genistein on ovarian dysfunction in a letrozole-induced PCOS mouse model, focusing on steroidogenesis, apoptosis, and PARP-1 signaling.
METHODS: PCOS was induced by oral administration of letrozole (37.5 mg/kg.day) for 21 days. Mice were then divided into the following three groups (n = 10 each) for another 21-day treatment: control (corn oil), PCOS (continued letrozole), and PCOS + GEN (letrozole + genistein, 50 mg/kg.day, i.p.).
KEY RESULTS: Genistein restored estrous cyclicity in 80% of treated mice versus 0% in the PCOS group (P < 0.05). Histologically, it improved follicular morphology, increased granulosa cell thickness and density, and promoted corpora lutea formation. Genistein significantly reduced serum T and P4 concentrations (P < 0.05) and modulated expression of steroidogenic proteins (CYP11A1, CYP19A1, STAR). It also decreased cleaved Caspase-3 and cleaved PARP-1 expression (P < 0.05), and suppressed abnormal PARylation without affecting total PARP-1 expression levels.
CONCLUSIONS: Genistein alleviates ovarian dysfunction in PCOS mice by restoring estrous cyclicity, enhancing follicular development, and normalizing hormone concentrations, through regulation of steroidogenic proteins, inhibition of apoptosis, and modulation of PARP-1 activity.
IMPLICATIONS: These findings support genistein as a potential therapeutic agent for PCOS, targeting the PARP-1-pADPr axis and apoptosis. Further studies are needed to explore upstream mechanisms and evaluate its long-term effects on reproductive health.