Polyphyllin I inhibits endometriosis in vitro by inducing apoptosis and autophagy via the inactivation of AKT/mTOR signalling pathway

Liping Li, Qiwen Hu, Jin Chen, Xiumei Zhang, Jinhua Wang, Yong Luo
Natural product research · 2025 · vol. 39(5) , pp. 1095–1100 · doi:10.1080/14786419.2023.2294113 · PMID:38099370
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Polyphyllin I reduces ectopic endometrial stromal cell viability, motility, and migration by inducing apoptosis and autophagy through inactivation of the AKT/mTOR pathway.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-08 · read from full text ⓘ

This study examined whether Polyphyllin I (PPI) affects ectopic endometrial stromal cells (EESCs) in vitro, using CCK-8 and flow cytometry to assess viability and apoptosis, and wound-healing and transwell assays to evaluate migration. The authors found that PPI reduced EESC viability and increased the proportion of apoptotic cells in a dose-dependent manner, alongside decreased cell motility and migration. Western blot results showed reduced p62 and increased LC3-II, consistent with autophagy induction, and also demonstrated decreased phosphorylated Akt and mTOR with rising PPI concentrations to link the effects to inactivation of the AKT/mTOR signaling pathway; a stated limitation is that the work was performed in vitro without additional in vivo validation reported. This paper is centrally about endometriosis — specifically, it tests PPI’s in vitro anti-endometriosis effects on ectopic endometrial stromal cells via apoptosis, autophagy, and AKT/mTOR pathway inactivation.

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Abstract

Previous research has indicated that Polyphyllin I (PPI) possesses potent anticancer properties. However, its impact on endometriosis remains unexplored. This study aims to investigate the inhibitory effects of PPI on ectopic endometrial stromal cells (EESCs). The CCK-8 and flow cytometry results respectively showed that the cell viability of EESCs decreased and the number of apoptotic cells increased in a dosage dependent of PPI. Wound healing and transwell assays demonstrated a notable reduction in cell motility and migration ability in the PPI group. Moreover, the Western blot analysis revealed a decrease in p62 levels and an increase in LC3-II expression following PPI administration. Additionally, the protein levels of p-Akt and p-mTOR were observed to decrease with increasing concentrations of PPI, indicating the potential of PPI to induce autophagy in EESCs through modulation of the Akt/mTOR signalling pathway. Consequently, PPI holds promise as a targeted therapeutic agent for the management of endometriosis.
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Abstract Previous research has indicated that Polyphyllin I (PPI) possesses potent anticancer properties. However, its impact on endometriosis remains unexplored. This study aims to investigate the inhibitory effects of PPI on ectopic endometrial stromal cells (EESCs). The CCK-8 and flow cytometry results respectively showed that the cell viability of EESCs decreased and the number of apoptotic cells increased in a dosage dependent of PPI. Wound healing and transwell assays demonstrated a notable reduction in cell motility and migration ability in the PPI group. Moreover, the Western blot analysis revealed a decrease in p62 levels and an increase in LC3-II expression following PPI administration. Additionally, the protein levels of p-Akt and p-mTOR were observed to decrease with increasing concentrations of PPI, indicating the potential of PPI to induce autophagy in EESCs through modulation of the Akt/mTOR signalling pathway. Consequently, PPI holds promise as a targeted therapeutic agent for the management of endometriosis. Disclosure statement No potential conflict of interest was reported by the authors.

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Condition tags

endometriosis

MeSH descriptors

Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Apoptosis Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy

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