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菟丝子总黄酮通过MAPK信号通路抗流产的作用

Effect of Total Flavones from Cuscuta Chinensis on Anti-Abortion via the MAPK Signaling Pathway.

作者信息

Wu Hai-Wang, Feng Yi-Hui, Wang Dong-Ying, Qiu Wei-Yu, Yu Qing-Ying, Yang Li-Lin, Liang Chun, Luo Song-Ping, Gao Jie

机构信息

Guangzhou University of Chinese Medicine, Guangzhou, China.

Division of Life Science, Center for Cancer Research and State Key Lab for Molecular Neural Science, Hong Kong University of Science and Technology, Hong Kong, China.

出版信息

Evid Based Complement Alternat Med. 2018 Oct 2;2018:6356190. doi: 10.1155/2018/6356190. eCollection 2018.

DOI:10.1155/2018/6356190
PMID:30369955
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6189658/
Abstract

For centuries, the Chinese herb Cuscuta chinensis has been applied clinically for abortion prevention in traditional Chinese medicine (TCM). Total flavones extracted from Cuscuta chinensis (TFCC) are one of the active components in the herb and also display anti-abortion effect similar to the unprocessed material. However, how TFCC exerts the anti-abortion effect remains largely unknown. In this study, we aim at characterizing the anti-abortion effects of TFCC and its underlying molecular mechanism in vitro and in vivo using human primary decidua cells and a mifepristone-induced abortion model in rat, respectively. The damage to the decidua caused by mifepristone in vivo was reversed by TFCC treatment in a dosage-dependent manner. High dosage of TFCC significantly upregulated the expression of estrogen receptor (ER), progesterone receptor (PR), and prolactin receptor (PRLR) in decidua tissue but downregulated the expression of p-ERK. Furthermore, we detected higher level of p-ERK and p-p38 in primary decidua cells from spontaneous abortion while treatment by TFCC downregulated their expression. Our results suggest TFCC mediates its anti-abortion effect by interfering with MAPK signaling pathway.

摘要

几个世纪以来,中药菟丝子一直在临床上用于预防流产。从菟丝子中提取的总黄酮(TFCC)是该草药的活性成分之一,并且也显示出与未加工材料相似的抗流产作用。然而,TFCC如何发挥抗流产作用在很大程度上仍然未知。在本研究中,我们旨在分别使用人原代蜕膜细胞和米非司酮诱导的大鼠流产模型,在体外和体内表征TFCC的抗流产作用及其潜在的分子机制。TFCC处理以剂量依赖性方式逆转了米非司酮在体内对蜕膜造成的损伤。高剂量的TFCC显著上调了蜕膜组织中雌激素受体(ER)、孕激素受体(PR)和催乳素受体(PRLR)的表达,但下调了p-ERK的表达。此外,我们在自然流产的原代蜕膜细胞中检测到较高水平的p-ERK和p-p38,而TFCC处理下调了它们的表达。我们的结果表明,TFCC通过干扰丝裂原活化蛋白激酶(MAPK)信号通路介导其抗流产作用。

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