Wen Mingxiao, Chen Wenjun, Zhou Qun, Dou Xiaoqing
Department of Gynaecology and Obstetrics, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Traditional Chinese Medicine), Hangzhou 310000, China.
Iran J Basic Med Sci. 2022 Jul;25(7):882-889. doi: 10.22038/IJBMS.2022.64475.14179.
Astragaloside IV (AS-IV) is a bioactive saponin with a wide range of pharmacological effects. This study was aimed at investigating its potential effect on polycystic ovary syndrome (PCOS).
Female Sprague-Dawley rats were randomly divided into five groups (control, PCOS, PCOS+AS-IV 20 mg/kg, PCOS+AS-IV 40 mg/kg, and PCOS+AS-IV 80 mg/kg). The pathological injury level of rat ovary was observed with hematoxylin-eosin (H&E) staining; enzyme-linked immunosorbent assay (ELISA) kit was utilized to measure the levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone in rat serum; western blot detected autophagy-associated or peroxisome proliferator-activated receptor γ (PPARγ) pathway-related protein expression; immunofluorescence was performed to observe LC3 level in rat ovarian tissue. After co-treatment with AS-IV and PPARγ inhibitor, the proliferation in ovarian granulosa cell line KGN was examined employing cell counting kit-8 (CCK-8), EdU staining, and colony formation; cell apoptosis was observed with TdT-mediated dUTP nick-end labeling (TUNEL); apoptosis-related protein expression was assayed by western blot.
Treatment with AS-IV inhibited the ovarian pathological damage in PCOS rats. It also promoted the level of autophagy and activated PPARγ signaling in the rat PCOS model. In KGN cells, the level of autophagy and expression of PPARγ-related proteins were also elevated by AS-IV treatment. Furthermore, AS-IV facilitated autophagy, thus inhibiting KGN cell proliferation and promoting its apoptosis, through activating the PPARγ signaling pathway.
AS-IV-activated PPARγ inhibits proliferation and promotes the apoptosis of ovarian granulosa cells, enhancing ovarian function in rats with PCOS.
黄芪甲苷IV（AS-IV）是一种具有广泛药理作用的生物活性皂苷。本研究旨在探讨其对多囊卵巢综合征（PCOS）的潜在影响。
将雌性Sprague-Dawley大鼠随机分为五组（对照组、PCOS组、PCOS+AS-IV 20mg/kg组、PCOS+AS-IV 40mg/kg组和PCOS+AS-IV 80mg/kg组）。采用苏木精-伊红（H&E）染色观察大鼠卵巢的病理损伤程度；利用酶联免疫吸附测定（ELISA）试剂盒检测大鼠血清中黄体生成素（LH）、卵泡刺激素（FSH）和睾酮的水平；蛋白质免疫印迹法检测自噬相关或过氧化物酶体增殖物激活受体γ（PPARγ）通路相关蛋白的表达；进行免疫荧光观察大鼠卵巢组织中LC3水平。在AS-IV与PPARγ抑制剂联合处理后，采用细胞计数试剂盒-8（CCK-8）、EdU染色和集落形成实验检测卵巢颗粒细胞系KGN的增殖情况；用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法（TUNEL）观察细胞凋亡；通过蛋白质免疫印迹法检测凋亡相关蛋白的表达。
AS-IV处理可抑制PCOS大鼠的卵巢病理损伤。它还能提高大鼠PCOS模型中的自噬水平并激活PPARγ信号通路。在KGN细胞中，AS-IV处理也能提高自噬水平和PPARγ相关蛋白的表达。此外，AS-IV通过激活PPARγ信号通路促进自噬，从而抑制KGN细胞增殖并促进其凋亡。
AS-IV激活PPARγ可抑制卵巢颗粒细胞增殖并促进其凋亡，改善PCOS大鼠的卵巢功能。
