Lidocaine Protects Endometriosis by Inducing Apoptosis of Endometrial Stromal Cells

Objective: This study aimed to explore the effects of lidocaine on ectopic endometrial stromal cells and the underlying mechanisms in endometriosis. Methods: Ectopic endometrial stromal cells (ESCs), which were separated from endometriotic tissues, were subjected to various concentrations of lidocaine for different time. After the treatment of lidocaine, MTT assay was applied to assess the cell proliferation of ESCs, and cell apoptosis was analyzed by flow cytometry. Meanwhile, we detected the protein level of pro-caspse3 and cleaved-caspase3 protein in ESCs by Western blot analysis. The invasion and migration capability of ESCs was also detected by transwell assay. Western blot analysis and qRT-PCR were performed for the detection of EMT markers (E-cadherin, N-cadherin and MMP-9). Similarly, the expression levels of β -catenin, cyclin D1 and c-myc in ESCs were determined by Western blot analysis and qRT-PCR. Results: 0.5, 1, 5 and 10 mM of lidocaine obviously inhibited the cell proliferation of ESCs at different time points compared with the control group, while no significant effect was observed in 0.1 mM lidocaine treated cells. Lidocaine dose-dependently increased cell apoptosis, reduced the protein level of pro-caspse3 protein, but improved cleaved-caspase3 protein level in ESCs. Moreover, lidocaine dose-dependently decreased the migration and invasion capabilities of ESCs. In addition, compared to the control group, lidocaine enhanced the level of E-cadherin, and reduced the level of N-cadherin and MMP-9 in ESCs. Lidocaine suppressed the level of β -catenin, cyclin D1 and c-myc in ESCs in a dose-dependent manner. Conclusion: We demonstrated that lidocaine protected endometriosis by inducing the apoptosis of ESCs via regulating Wnt/ β -catenin pathway.