Department of Educational Management, China Academy of Chinese Medical Science, Beijing 100007, China.
Xiyuan Hospital, China Academy of Chinese Medical Science, Beijing 100091, China.
J Tradit Chin Med. 2022 Feb;42(1):23-29. doi: 10.19852/j.cnki.jtcm.2022.01.002.
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.
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.
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).
BCD treatment could attenuate pathological process in POI ovaries, suppress GC apoptosis, probably through promoting BMP-7 expression and following inhibiting caspase-3 activation.
研究补肾促卵方对雷公藤多苷致卵巢早衰（POI）模型小鼠卵巢卵泡及颗粒细胞的保护作用，并探讨其作用机制。
80 只雌性 Balb/c 小鼠随机分为 4 组（n=20）：空白组、模型组、补肾促卵方组（BCD 组）和戊酸雌二醇组（EV 组）。在造模的第 14 天，模型组、BCD 组和 EV 组小鼠给予雷公藤多苷灌胃建立 POI 模型。在治疗的第 14 天，BCD 组小鼠给予补肾促卵方 18.35mg·kg-1·d-1，EV 组小鼠给予戊酸雌二醇溶液 0.15mg·kg-1·d-1，空白组和模型组小鼠给予生理盐水。治疗完成后，采集全血检测血清卵泡刺激素（FSH）、黄体生成素（LH）、雌二醇（E2）、抗苗勒管激素（AMH）水平和血管内皮生长因子（VEGF）、骨形成蛋白-7（BMP-7）。采集卵巢组织进行形态学观察、卵泡计数、卵巢颗粒细胞凋亡检测及 BMP-7、caspase-3 表达检测。
除雷公藤多苷干预阶段外，各组小鼠体重均稳定增长。与模型组比较，BCD 组小鼠卵巢指数、血清 E2、AMH、VEGF、BMP-7 水平升高，FSH 水平降低（P<0.05）；与 EV 组比较，BCD 组 VEGF 水平升高（P<0.05）。与模型组比较，BCD 组小鼠卵巢组织病理损伤减轻，GC 凋亡减少，窦前卵泡计数、BMP-7 表达上调，caspase-3 表达下调（P<0.05）。
补肾促卵方可改善 POI 卵巢的病理损伤，抑制 GC 凋亡，其机制可能与上调 BMP-7 表达，抑制 caspase-3 激活有关。
