SCM-198 Prevents Endometriosis by Reversing Low Autophagy of Endometrial Stromal Cell via Balancing ERα and PR Signals

Yikong Lin, Yi-Kong Lin, Yunyun Li, Yun-Yun Li, Yue Li, Da-Jin Li, Da‐Jin Li, Xiao-Lin Wang, Xiaolin Wang, Li Wang, Min Yu, Yi Zhun Zhu, Yi-Zhun Zhu, Jia-Jing Cheng, Mei-Rong Du, Meirong Du
Frontiers in endocrinology · 2022 · vol. 13 , pp. 858176 · doi:10.3389/fendo.2022.858176 · PMID:35784569 · PMC9245568 · W4283018542
article OA: gold CC0 ⤵ 10 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

SCM-198 reverses low autophagy in endometriosis stromal cells by balancing ERα and PR signaling, thus inhibiting ectopic lesion growth and promoting apoptosis.

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

This study evaluated whether SCM-198, a synthetic leonurine derivative, can inhibit endometriosis progression and investigated its mechanism by using an estradiol/mince-induced endometriosis mouse model alongside RNA-seq, ELISA, western blotting, and in vitro experiments with normal and ectopic endometrial stromal cells. The authors report that ectopic stromal cells show increased ERα signaling, decreased PRB expression, and consequently low autophagy, which together support ectopic cell survival and antiapoptotic effects; elevated TNF-α further reinforces this via aromatase–estrogen–ERα signaling. SCM-198 reduced ectopic lesion growth in vivo and increased apoptosis in vitro and in vivo by restoring autophagy through TNF-α–aromatase–estrogen–ERα inhibition and PRB upregulation. A stated limitation is that the work relies on mouse/isolated cell models and a specific experimental EMS induction approach rather than established clinical endpoints. This paper is centrally about endometriosis — specifically, SCM-198’s regulation of the inflammation–endocrine–autophagy axis involving ERα, PRB, TNF-α, aromatase, and autophagy in ectopic endometrial stromal cells.

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Abstract

BACKGROUND: Endometriosis (EMS), an endocrine-related inflammatory disease, is characterized by estrogen and progesterone imbalance in ectopic lesions. However, its pathogenic mechanism has not been fully elucidated. While SCM-198 is the synthetic form of leonurine and has multiple pharmacological activities such as antioxidation and anti-inflammation, it remains unknown whether it could inhibit the progress of EMS by regulating estrogen signaling and inflammation. METHODS: The therapeutic effects of SCM-198 on EMS and its potential mechanism were analyzed by establishing EMS mouse models and performing an RNA sequencing (RNA-seq) assay. ELISA was performed to detect estrogen and tumor necrosis factor (TNF) -α concentrations in normal endometrial stromal cells (nESCs) and ectopic endometrial stromal cells (eESCs) with or without SCM-198 treatment. Western blotting, RNA silencing, and plasmid overexpression were used to analyze the relationship between inflammation, endocrine factors, and autophagy and the regulatory activity of SCM-198 on the inflammation-endocrine-autophagy axis. RESULTS: Increased estrogen-estrogen receptor (ER) α signaling and decreased progesterone receptor isoform B (PRB) expression synergistically led to a hypo-autophagy state in eESCs, which further inhibited the apoptosis of eESCs. The high expression of TNF-α in eESCs enhanced the antiapoptotic effect mediated by low autophagy through the activation of the aromatase-estrogen-ERα signaling pathway. SCM-198 inhibited the growth of ectopic lesions in EMS mice and promoted the apoptosis of eESCs both in vivo and in vitro. The apoptotic effect of SCM-198 on eESCs was attained by upregulating the autophagy level via the inhibition of the TNF-α-activated aromatase-estrogen-ERα signal and the increase in PRB expression. CONCLUSION: Inflammation facilitated the progress of EMS by disrupting the estrogen regulatory axis. SCM-198 inhibited EMS progression by regulating the inflammation-endocrine-autophagy axis.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis

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