首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >Danggui Buxue Tang Rescues Folliculogenesis and Ovarian Cell Apoptosis in Rats with Premature Ovarian Insufficiency
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Danggui Buxue Tang Rescues Folliculogenesis and Ovarian Cell Apoptosis in Rats with Premature Ovarian Insufficiency

机译:Danggui Buxue唐拯救过早卵巢功能不全的大鼠卵泡发生和卵巢细胞凋亡

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Premature ovarian insufficiency (POI) is a common female endocrine disease that is closely linked to ovarian function. Danggui Buxue Tang (DBT) is a classic prescription of traditional Chinese medicine that is helpful for rescuing ovarian function. However, the mechanism by which DBT rescues ovarian function remains unclear. This study explored the molecular mechanism of DBT with respect to apoptosis and related signals in ovarian cells. The quality control of DBT was performed by HPLC. After DBT intervention in the POI rat model, serum AMH/FSH/LH/E 2 levels were detected by ELISA, follicles at various developmental stages were observed by HE staining, apoptosis was detected by TUNEL, and the expression profiles of Bcl-2 family proteins and key proteins in the Jak2/Foxo3a signaling pathway were evaluated by western blot. The results demonstrated that DBT could encourage the development of primary/secondary/antral follicles and increase the secretion of AMH. Moreover, DBT might inhibit Foxo3a by upregulating Jak2, thereby mediating Bcl-2 family activities and inhibiting apoptosis in ovarian cells. In conclusion, DBT promotes follicular development and rescues ovarian function by regulating Bcl-2 family proteins to inhibit cell apoptosis, which could be related to the Jak2/Foxo3a signaling pathway.
机译:过早的卵巢不足(POI)是一种与卵巢功能密切相关的常见的女性内分泌疾病。 Danggui Buxue Tang(DBT)是一种经典的中药,有助于救援卵巢功能。然而,DBT救援卵巢功能仍然不清楚的机制仍不清楚。该研究探讨了DBT关于卵巢细胞中凋亡和相关信号的分子机制。通过HPLC进行DBT的质量控制。在POI大鼠模型中进行DBT干预后,ELISA检测到血清AMH / FSH / LH / LH / LH / LH / E 2水平,通过染色观察到各种发育阶段的卵泡,由TUNEL检测到细胞凋亡,以及BCL-2家族的表达谱检测通过Western印迹评估JAK2 / FOXO3A信号传导途径中的蛋白质和键蛋白。结果表明,DBT可以促进初级/仲/嗜睡卵泡的发育,并增加AMH的分泌。此外,DBT可以通过上调JAK2来抑制FOXO3A,从而介导BCL-2家族活动并抑制卵巢细胞中的凋亡。总之,DBT通过调节BCL-2家族蛋白来抑制细胞凋亡,促进卵巢发育并拯救卵巢功能,这可能与JAK2 / FOXO3A信号通路有关。

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