Zearalenone affects the growth of endometriosis via estrogen signaling and inflammatory pathways

Wan-Kun Yan, Wan‐Kun Yan, Ying-Nan Liu, Yingnan Liu, Shan-Shan Song, Shanshan Song, Jinwen Kang, Jin-Wen Kang, Yu Zhang, Lei Lu, Shu‐Wen Wei, Shu-Wen Wei, Qixin Xu, Qi-Xin Xu, Wang‐Qing Zhang, Wang-Qing Zhang, Xiao‐Zheng Liu, Xiao-Zheng Liu, Yao Wu, Ren-Wei Su, Ren‐Wei Su
Ecotoxicology and environmental safety · 2022 · vol. 241 , pp. 113826 · doi:10.1016/j.ecoenv.2022.113826 · PMID:36068753 · W4283735010
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Zearalenone inhibited endometriosis growth in mice by reducing cell proliferation, increasing apoptosis, impairing estrogen signaling, and suppressing inflammatory pathways, but acted estrogenically in estrogen-deficient conditions.

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Abstract

Endometriosis is a chronic, inflammatory, estrogen-dependent gynecological disease characterized by the growth of endometrial stromal cells and glands outside the uterine cavity in response to hormones, which commonly occurs in reproductive-age women. Zearalenone (ZEA) is a toxic metabolite produced by Fusarium, which acts as estrogen activity because of the similarity of its structure to estrogen. In this study, we used an endometriosis mouse model: 15 days after ovariectomy, endometrial fragments were sutured on the pelvic wall, and exogenous estrogen was supplied using an estrogen-releasing silicone tube embedded subcutaneously. Mice were treated with different doses of ZEA by gavage for 21 days. The results show that ZEA significantly inhibited the growth of ectopic endometrium in a dose-dependent manner. The proliferation of cells decreased while apoptosis increased in the ectopic tissues of ZEA-treated mice compared to the vehicle group. The expression of estrogen receptor-α and its downstream targets MUC1 and p-AKT decreased, indicating an impaired estrogen signaling activity by ZEA treatment. In addition, the decreased expression of pro-inflammatory cytokine Tnf-α, Il-1β, and Il-6, the lower number of macrophages and neutrophils cells, and the inhibited NF-κB signaling pathway suggest the inflammatory response in the ectopic endometrium was also suppressed by ZEA treatment. However, when the exogenous estrogen supply is removed, ZEA, in turn, plays an estrogen-like role that promotes cell proliferation in the ectopic endometrium. In summary, our data suggest ZEA acts as an antagonist in endometriotic tissue when estrogen is sufficient but turns to estrogenic activity in the absence of estrogen in the development of endometriosis. ZEA also inhibits ectopic tissue growth by inhibiting inflammatory response in the endometriosis model.

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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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