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

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.