SCM-198 Alleviates Endometriosis by Suppressing Estrogen-ERα mediated Differentiation and Function of CD4+CD25+ Regulatory T Cells

Yunyun Li, Yun-Yun Li, Yi-Kong Lin, Yikong Lin, Yue Li, Xin-Hua Liu, Xinhua Liu, Da‐Jin Li, Da-Jin Li, Xiaolin Wang, Xiao-Lin Wang, Li Wang, Yi Zhun Zhu, Yi-Zhun Zhu, Min Yu, Meirong Du, Mei-Rong Du
International journal of biological sciences · 2022 · vol. 18(5) , pp. 1961–1973 · doi:10.7150/ijbs.68224 · PMID:35342349 · W4212838624
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

SCM-198 suppresses estrogen-ERα mediated differentiation and function of CD4+CD25+ regulatory T cells to alleviate endometriosis growth and ectopic lesion development.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This paper studied how SCM-198, a synthetic leonurine derivative, affects regulatory T cells (Tregs) and estrogen/estrogen receptor α (ERα) signaling in endometriosis. The authors analyzed peritoneal fluid from women with endometriosis (and non-endometriosis controls) using flow cytometry and measured peritoneal estrogen levels and ERα/ERβ mRNA in Tregs, then used in vitro induction, co-culture/invasion and viability assays, and an endometriosis mouse model to test whether SCM-198 modulates estrogen-ERα–driven Treg expansion and function. They found increased Tregs in endometriosis peritoneal fluid with estrogen-ERα overactivation, that estrogen-ERα increased Treg cytokines IL-10 and TGF-β1 in a way reversed by SCM-198, and that SCM-198 reduced the invasion and viability of ectopic endometrial stromal cells enhanced by Tregs, with in vivo results showing smaller ectopic lesions and downregulated Treg functions via estrogen-ERα inactivation. The paper’s limitation is that it excludes adenomyosis and other pelvic conditions from human sampling, which may restrict generalizability beyond isolated endometriosis. This paper is centrally about endometriosis — SCM-198 alleviates endometriosis by suppressing estrogen–ERα–mediated differentiation/function of CD4+CD25+ Tregs.

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Abstract

Background: Endometriosis (EMS), a typical endocrine immune disorder, associates with dramatically increased estrogen production and disorganized immune response in ectopic focus. Peritoneal regulatory T cells (Tregs) expansion in women with EMS and their pathogenic role attributable to endometriotic immunotolerance has been reported. Whether local high estrogen promotes EMS by discipling Tregs needs to be further explored. Up to date, there is no effective medicine for the treatment of EMS. SCM-198 is a synthetic leonurine with multiple physiological activities. Whether SCM-198 could regulate Tregs via estrogen and facilitate the radical cure of EMS has not yet been reported. Methods: Proportion of Tregs in peritoneal fluid of patients with EMS was firstly analyzed via flow cytometry. Peritoneal estrogen concentration and the mRNA levels of estrogen receptor (ER) and estrogen receptor (ER) of Tregs were detected by ELISA and RT-PCR, respectively. Grouped in vitro induction assays were performed to explore the effects of SCM-198 and estrogen signaling on Tregs. Cell invasion and viability assays were utilized to detect the crosstalk between Tregs and ectopic endometrial stromal cells (eESCs), with or without SCM-198 treatment. Furthermore, EMS mice models were established to verify the therapeutic effects of Results: Increased Tregs were found in peritoneal fluid of EMS patients, accompanied with estrogen-ER overactivation. Estrogen-ER triggered the expansion of Tregs and their cytokine production (IL-10 and TGF-1), which could be reversed by SCM-198 treatment. Moreover, SCM-198 abated the invasion and viability of eESCs enhanced by Tregs. In vivo experiments confirmed that SCM-198 obviously retarded the growth of ectopic lesions and downregulated the functions of Tregs via estrogen-ER inactivation.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Estrogen Receptor alpha Estrogen Receptor alpha Estrogen Receptor alpha Estrogen Receptor alpha Animals Animals Animals Estrogens Estrogens Estrogens Female Female Female Gallic Acid Gallic Acid

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