Efficacy of Bushen Culuan decoction on ovarian follicle and follicular granulosa cells in mice with premature ovarian insufficiency induced by tripterygium wilfordii polyglycoside.
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Bushen Culuan decoction treatment attenuated premature ovarian insufficiency in mice by suppressing granulosa cell apoptosis, likely via promoting BMP-7 and inhibiting caspase-3.
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Abstract
OBJECTIVE: To investigate the protective efficacy of Bushen Culuan decoction (BCD) on ovarian follicle and follicular granulosa cells in mice with premature ovarian insufficiency (POI) induced by tripterygium wilfordii polyglycoside, and to study the potential mechanism underlying the action. METHODS: Eighty female Balb/c mice were randomly divided into 4 groups (n = 20 each): blank group, model group, Bushen Culuan decoction intervening group (BCD group) and estradiol valerate intervening group (EV group). In the first 14 model establishing d, mice in model group, BCD group and EV group were under Tripterygium wilfordii polyglycoside (TWP) gavage to establish POI models. In the 14-day therapeutic stage, mice in BCD group were taken BCD 18.35 mg·kg-1d-1, mice in EV group were taken EV solution 0.15 mg·kg-1d-1, while mice in blank group and model group were taken normal saline. When the mice accomplished therapy, whole blood was collected for serum hormone including follicle stimulating hormone (FSH), luteal hormone (LH), estradiol (E2), antimullerian hormone (AMH) levels and vascular endothelial growth factor (VEGF), bone morphogenetic protein-7 (BMP-7) measurement. Ovarian tissues were harvested for morphologic observation, follicle counting, ovarian follicular graulosa cell apoptosis test and testing BMP-7 and caspase-3 expressions. RESULTS: The body weights of the mice kept growing stably in the process expect in TWP intervening stage. Compared with model group, BCD group had significantly higher ovarian index, serum E2, AMH, VEGF, BMP-7 levels and significantly lower FSH level (P < 0.05). Meanwhile the VEGF level in BCD group was higher than in EV group (P < 0.05). Compared with model group, the histopathological damage and GCs apoptosis were mitigated; developing follicle counting, BMP-7 expression were up-regulated, and caspase-3 expression was downregulated in BCD groups (P < 0.05). CONCLUSION: BCD treatment could attenuate pathological process in POI ovaries, suppress GC apoptosis, probably through promoting BMP-7 expression and following inhibiting caspase-3 activation.
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