Paeonol alleviates migration and invasion of endometrial stromal cells by reducing HIF-1α-regulated autophagy in endometriosis

Conghui Pang, Zhijuan Wu, Zhi-Juan Wu, Xiaoyan Xu, Wenxiu Yang, Xiaoxuan Wang, Yinghua Qi
Frontiers in bioscience (Landmark edition) · 2021 · vol. 26(9) , pp. 485–495 · doi:10.52586/4961 · PMID:34590461 · W3203430457
article OA: gold CC0 ⤵ 12 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Paeonol reduced the migration and invasion of endometrial stromal cells by inhibiting HIF-1α-regulated autophagy, thereby attenuating endometriotic lesion formation.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-09 ⓘ

This study investigated whether paeonol affects hypoxia-driven migration and invasion of ectopic endometrial stromal cells (ecESCs) derived from ovarian endometriosis patients, using in vitro assays (cell viability/proliferation, apoptosis, wound healing, and Matrigel transwell) and measurements of hypoxia/HIF-1α–linked autophagy markers (LC3-II/LC3-I, Beclin-1, and p62). Paeonol reduced ecESC proliferation and metastasis under hypoxia and increased apoptosis, while it repressed hypoxia-induced autophagy in ecESCs, accompanied by decreased LC3 and Beclin-1 and increased p62, with the authors also examining HIF-1α overexpression to support a mechanistic link between HIF-1α, autophagy, and invasive behavior. In a rat endometriosis model, paeonol ameliorated endometriotic lesion histopathology and altered inflammatory cytokine levels (IL-1β is mentioned) alongside changes in HIF-1α/autophagy-related proteins. The study’s main limitations include the small patient sample (N=7) and reliance on cell and rat models to represent human endometriosis, even though tissues and cells were clinically sourced. This paper is centrally about endometriosis — it specifically tests paeonol’s effects on ecESC migration/invasion and HIF-1α-regulated autophagy in ovarian endometriosis.

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Abstract

Background: Dysregulated migration and invasion of endometrial stromal cells is implicated in the pathogenesis of endometriosis. Hypoxia functions as critical microenvironmental factor that results in promotion of endometrial stromal cells migration and invasion through up-regulation of autophagy. Paeonol functioned as a tumor suppressor in human ovarian cancer and promoted cytoprotective autophagy. However, the role of paeonol in hypoxia-induced autophagy in endometriosis remains unknown. Methods: Stromal cells were isolated from endometriotic patients by enzymatic digestion of ectopic endometrial tissues, and then characterized by immunohistochemical analysis of cytoskeleton 19 (CK19) and vimentin. Cellular morphology was evaluated under microscope. Cell viability, proliferation and apoptosis of stromal cells were assessed by Cell Counting Kit-8, EdU labeling and flow cytometry, respectively. Wound healing and transwell assays were performed to detect metastasis of the stromal cells. Hypoxia-induced autophagy was evaluated through immunohistochemistry and western blot. Results: Paeonol treatment dosage dependently decreased cell proliferation and metastasis of the ectopic endometrial stromal cells (ecESCs), while promoted the cell apoptosis. Hypoxia-induced autophagy in the ecESCs was repressed by paeonol through down-regulation of LC3-II/LC3-I and Beclin-1, while up-regulation of p62. Hypoxia-inducible factor-1α (HIF-1α) was reduced post paeonol treatment, and paeonol-induced increase of p62 and decrease of LC3-II/LC3-I and Beclin-1 were reversed by over-expression of HIF-1α. Over-expression of HIF-1α also attenuated the suppressive effect of paeonol on cell growth of ecESCs. Conclusions: Paeonol attenuated HIF-1α-induced promotion of ecESCs migration and invasion through reducing autophagy, and reduced HIF-1α-induced endometriotic lesion in rats, providing potential therapeutic strategy for the treatment of endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Acetophenones Animals Autophagy Endometrium Female Humans Hypoxia-Inducible Factor 1, alpha Subunit Hypoxia-Inducible Factor 1, alpha Subunit Rats Stromal Cells

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