Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

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

Fenyun Zhang¹, Qianqian Wang²

¹Department of Obstetrics and Gynecology, Hangzhou Ninth Peopleâ€™s Hospital, Hangzhou, Zhejiang Province 311200, China; ²Center for Reproductive Medicine, Department of Obstetrics, Zhejiang Provincial Peopleâ€™s Hospital, Hangzhou Medical College, Hangzhou, Zhejiang Province 310000, China.

For correspondence:- Qianqian Wang Email: wangqianqian_dr@163.com Tel:+8657185893328

Accepted: 30 October 2022 Published: 30 November 2022

Citation: Zhang F, Wang Q. Ellipticine induces apoptosis and mitochondrial dysfunction in human endometriosis cell lines by activating MAPK signaling pathway. Trop J Pharm Res 2022; 21(11):2353-2358 doi: 10.4314/tjpr.v21i11.12

© 2022 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

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

Keywords: Endometriosis, Ellipticine (EPT), Apoptosis, Mitochondrial damage, MAPK pathway