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吴茱萸碱通过抑制雌激素受体β（ERβ）来抑制早期EB病毒暴露诱导的子宫内膜异位症发展。

Evodiamine suppresses endometriosis development induced by early EBV exposure through inhibition of ERβ.

作者信息

Wang Junling, Liang Yuanqi, Liang Xiaoru, Peng Huijuan, Wang Yongxia, Xu Mingtao, Liang Xuefang, Yao Helen, Liu Xiaohan, Zeng Liqin, Yao Paul, Xiang Dongfang

机构信息

Department of Gynecology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.

The Second Clinical College of Guangzhou University of Chinese Medicine, Guangzhou, China.

出版信息

Front Pharmacol. 2024 Aug 1;15:1426660. doi: 10.3389/fphar.2024.1426660. eCollection 2024.

DOI:10.3389/fphar.2024.1426660
PMID:39148548
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11324466/
Abstract

Endometriosis (EMS) is characterized as a prevalent gynecological inflammatory disorder marked by the existence of endometrial tissues situated beyond the uterus. This condition leads to persistent pelvic pain and may contribute to infertility. In this investigation, we explored the potential mechanism underlying the development of endometriosis (EMS) triggered by transient exposure to either latent membrane protein 1 (LMP1) or Epstein-Barr virus (EBV) in a mouse model. Additionally, we examined the potential inhibitory effect of evodiamine (EDM) on EMS. Immortalized human endometrial stromal cells (HESC) or epithelial cells (HEEC) were transiently exposed to either EBV or LMP1. The presence of evodiamine (EDM) was assessed for its impact on estrogen receptor β (ERβ) expression, as well as on cell metabolism parameters such as redox balance, mitochondrial function, inflammation, and proliferation. Additionally, a mixture of LMP1-treated HESC and HEEC was administered intraperitoneally to generate an EMS mouse model. Different dosages of EDM were employed for treatment to evaluate its potential suppressive effect on EMS development. Transient exposure to either EBV or LMP1 triggers persistent ERβ expression through epigenetic modifications, subsequently modulating related cell metabolism for EMS development. Furthermore, 4.0 µM of EDM can efficiently reverse this effect in cell culture studies. Additionally, 20 mg/kg body weight of EDM treatment can partly suppress EMS development in the EMS mouse model. Transient EBV/LMP1 exposure triggers permanent ERβ expression, favoring later EMS development, EDM inhibits EMS development through ERβ suppression. This presents a novel mechanism for the development of endometriosis (EMS) in adulthood stemming from early Epstein-Barr virus (EBV) exposure during childhood. Moreover, evodiamine (EDM) stands out as a prospective candidate for treating EMS.

摘要

子宫内膜异位症（EMS）是一种常见的妇科炎症性疾病，其特征是子宫外存在子宫内膜组织。这种病症会导致持续性盆腔疼痛，并可能导致不孕。在本研究中，我们在小鼠模型中探究了由短暂暴露于潜伏膜蛋白1（LMP1）或爱泼斯坦 - 巴尔病毒（EBV）引发子宫内膜异位症（EMS）发展的潜在机制。此外，我们研究了吴茱萸碱（EDM）对EMS的潜在抑制作用。将永生化的人子宫内膜基质细胞（HESC）或上皮细胞（HEEC）短暂暴露于EBV或LMP1。评估吴茱萸碱（EDM）对雌激素受体β（ERβ）表达的影响，以及对细胞代谢参数如氧化还原平衡、线粒体功能、炎症和增殖的影响。此外，将LMP1处理的HESC和HEEC混合物腹腔注射以建立EMS小鼠模型。采用不同剂量的EDM进行治疗，以评估其对EMS发展的潜在抑制作用。短暂暴露于EBV或LMP1会通过表观遗传修饰触发持续的ERβ表达，随后调节相关细胞代谢以促进EMS发展。此外，在细胞培养研究中，4.0 μM的EDM可以有效逆转这种效应。此外，20 mg/kg体重的EDM处理可部分抑制EMS小鼠模型中EMS的发展。短暂的EBV/LMP1暴露触发永久性ERβ表达，有利于后期EMS发展，EDM通过抑制ERβ抑制EMS发展。这为成年期子宫内膜异位症（EMS）的发展提出了一种新机制，该机制源于儿童期早期爱泼斯坦 - 巴尔病毒（EBV）暴露。此外，吴茱萸碱（EDM）是治疗EMS的一个有前景的候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ed/11324466/1906a0e9e25a/fphar-15-1426660-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ed/11324466/0ee7c26f6dfc/fphar-15-1426660-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ed/11324466/231f63a4a181/fphar-15-1426660-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ed/11324466/7ede164ad54a/fphar-15-1426660-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ed/11324466/cec4029ab06a/fphar-15-1426660-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ed/11324466/1906a0e9e25a/fphar-15-1426660-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ed/11324466/0ee7c26f6dfc/fphar-15-1426660-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ed/11324466/7ad503f8e606/fphar-15-1426660-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ed/11324466/231f63a4a181/fphar-15-1426660-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ed/11324466/4fb294eb6f19/fphar-15-1426660-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ed/11324466/7ede164ad54a/fphar-15-1426660-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ed/11324466/cec4029ab06a/fphar-15-1426660-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41ed/11324466/1906a0e9e25a/fphar-15-1426660-g008.jpg

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