Mechanisms of Traditional Chinese Medicine Bushenantai granules in promoting angiogenesis at the maternal-fetal interface of recurrent spontaneous abortion mice.

血管生成 血管内皮生长因子 内分泌学 医学 内科学 雌激素 孕酮受体 蜕膜 胎儿 雌激素受体 胚胎 血管内皮生长因子A 子宫内膜 免疫组织化学 男科 怀孕 生物 癌症 胎盘 血管内皮生长因子受体 乳腺癌 细胞生物学 遗传学
作者
Taijin Lan,Xuefei Luo,Ming-Yue Mo,Zhenxing Chen,Fei Luo,Siyin Han,Peng Liu,Zhongxiu Liang,Ting Zhang,Tianyi Li,Qiangqiang Yan,Yong Y. Lin,Jiang Lin
出处
期刊:PubMed [National Institutes of Health]
卷期号:41 (4): 556-563 被引量:9
标识
DOI:10.19852/j.cnki.jtcm.20210319.001
摘要

To assess the effects of Bushenantai (BSAT) granule() on angiogenesis-related factors [E2, P, and vascular endothelial growth factor (VEGF)] at the maternal-fetal interface of recurrent spontaneous abortion (RSA) mice, and to evaluate the role of BSAT in promoting angiogenesis at the maternal-fetal interface by influencing the expression of sex hormones, and VEGF.A mouse model with normal pregnancy and another with Clark's classic RSA were established. The RSA mice were randomly assigned to six groups: normal, model, progesterone, high-doseBSAT granule (BSAT-H), medium-dose-BSAT granule (BSAT-M), and low-dose-BSAT granule (BSAT-L) (n = 10 for each group). The embryo loss rate and the histopathological changes in the decidual tissues were measured. Serum levels of estrogen (E2), progesterone (P), and VEGF were detected by enzyme-linked immunosorbent assay. The mRNA and protein expressions of estradiol receptor (ER), progesterone receptor (PR), VEGF, and vascular endothelial growth factor receptor 2 (VEGFR2) in the decidual tissues were identified by immunohistochemistry, Western blotting, and quantitative reverse transcription polymerase chain reaction.The embryo loss rate in all groups that received BSAT treatment was reduced, while the number of blood vessels at decidual tissues was increased. The serum levels of E2, P and VEGF were elevated, and the mRNA and protein expressions of ER, PR, VEGF, and VEGFR2 in the decidual tissues were enhanced.BSAT can improve angiogenesis at the maternal-fetal interface and reduce the embryo loss rate, which may be associated with its ability to increase the serum levels of estrogen, progesterone, and VEGF, in addition to up-regulation of mRNA and protein expression of ER, PR, VEGF, and VEGFR2 in the decidual tissue.
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