Ellipticine induces apoptosis and mitochondrial dysfunction in human endometriosis cell lines by activating MAPK signaling pathway

Fenyun Zhang, Qianqian Wang
In: Tropical Journal of Pharmaceutical Research · 2023 · vol. 21(11) , pp. 2353–2358 · doi:10.4314/tjpr.v21i11.12 · W4323049393
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Ellipticine inhibited endometriosis cell viability and induced apoptosis and mitochondrial dysfunction by activating the MAPK signaling pathway in human endometriosis cell lines.

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⚙ AI-generated deep summary by qwen3.7-flash, 2026-08-27 · read from full text ⓘ

This study evaluated the alkaloid ellipticine as a potential therapeutic agent for endometriosis by testing its effects on human endometriosis-like cell lines. Researchers utilized flow cytometry, immunoblotting, and staining techniques to demonstrate that ellipticine significantly inhibited cell viability and stimulated apoptosis through mitochondrial damage. The findings indicate that these cytotoxic effects are mediated via the activation of the MAPK signaling pathway within the affected cells. While the results highlight ellipticine’s potential for managing endometriosis, the authors explicitly note that further in vivo studies are required to validate these observations. This paper is centrally about endometriosis — specifically investigating the molecular mechanisms by which ellipticine induces apoptosis in endometriosis cell lines.

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Abstract

Purpose: To assess the effect of ellipticine (EPT), an alkaloid isolated from the Oleaceae family, on endometriosis, and to identify its possible mechanisms of action. Methods: Human endometriosis-like cell lines exposed to EPT were subjected to bromodeoxyuridine/5-bromo-2´-deoxyuridine and proliferating cell nuclear antigen staining. Flow cytometry and immunoblot analyses were used to assess the effect of EPT on cell apoptosis. Mitochondrial damage was determined by JC-1 staining and immunoblotting. Immunoblot assays were performed to determine the effects of EPT on the MAPK pathway. Results: Ellipticine inhibited the viability of human endometriosis cell lines and stimulated cell apoptosis (p < 0.01). It further induced mitochondrial damage in human endometriosis cell lines (p < 0.01). Mechanistically, EPT acted on MAPK pathway, and induced apoptosis and mitochondrial dysfunction (p < 0.01) in human endometriosis cells. Conclusion: Ellipticine is a potential treatment strategy for the management of endometriosis. However, further exploration of this potential should be explored via in vivo studies.
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Abstract

Purpose: To assess the effect of ellipticine (EPT), an alkaloid isolated from the Oleaceae family, on endometriosis, and to identify its possible mechanisms of action.

Methods

Human endometriosis-like cell lines exposed to EPT were subjected to bromodeoxyuridine/5-bromo-2´-deoxyuridine and proliferating cell nuclear antigen staining. Flow cytometry and immunoblot analyses were used to assess the effect of EPT on cell apoptosis. Mitochondrial damage was determined by JC-1 staining and immunoblotting. Immunoblot assays were performed to determine the effects of EPT on the MAPK pathway.

Results

Ellipticine inhibited the viability of human endometriosis cell lines and stimulated cell apoptosis (p < 0.01). It further induced mitochondrial damage in human endometriosis cell lines (p < 0.01). Mechanistically, EPT acted on MAPK pathway, and induced apoptosis and mitochondrial dysfunction (p < 0.01) in human endometriosis cells.

Conclusion

Ellipticine is a potential treatment strategy for the management of endometriosis. However, further exploration of this potential should be explored via in vivo studies.

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endometriosis

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last seen: 2026-06-10T17:14:06.276822+00:00
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