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

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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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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