Protective role of propofol in endometriosis and its mechanism

Abstract

Endometriosis (EM) is a common benign gynecological disorder. The present study aimed to investigate the potential role of propofol, a commonly used intravenous anesthetic agent, in the pathogenesis of EM. The EM cell line CRL-7566 was used in the present study. CRL-7566 cells were first treated with various concentrations of propofol (0, 1, 5 or 10 μg/ml) for specific duration, and the cell viability and apoptotic rate were determined by performing an MTT and a flow cytometric cell apoptosis assay, respectively. The protein and mRNA levels of cell proliferation- and apoptosis-associated genes were detected by western blot and reverse-transcription quantitative polymerase chain reaction, respectively. The results demonstrated that propofol inhibited CRL-7566 cell proliferation in a dose- and time-dependent manner. CRL-7566 cell apoptosis was dose-dependently induced by propofol treatment. In addition, propofol treatment significantly increased the levels of forkhead box (FOX)O1, FOXO3, Bim, pro-caspase-3, active caspase-3, p53 and p21. In conclusion, the present study suggested that propofol inhibited the proliferation and induced apoptosis of EM cells via inducing the expression/activation of multiple associated genes/proteins, indicating a protective role of propofol in EM.