Effects of Aloe emodin on cell biological behaviors of human cervical carcinoma Hela cell in vitro

doi:10.3969/j.issn.1002-7386.2018.06.003

Abstract：Objective To investigate the effects of Aloe emodin (AE) on cell biological behaviors of cervical carcinoma Hela cell in vitro.Methods The cervical carcinoma Hela cells were cultured in vitro and treated with AE at the concentrations of 0,20,40,80,160μmol/L,respectively (experimental groups),moreover,the cells that were treated with the same volume DMSO instead of AE were served as control group. The cell proliferation state,cell cycle, cell apoptosis, cell migration and invasion abilities as well as the expression levels of Caspase-3 and Bcl-2 protein were observed and compared between two groups.Results As compared with those in control group, the inhibition effects of AE (10μmol/L) on cell proliferation were not obvious after 24 hour,however, with the time going on,the inhibition effects were gradually increased, and the inhibition effects of AE(20μmol/L) were significant(P<0.05).The IC50 of AE effects on Hela cells after 48 hours was 58.3μmol/L. On 48 hours after the cells were treated with AE,except for 10μmol/L concentration group, the cell proportion at G2/M phase of cell cycle in the other concentration groups was significantly increased,as compared with that in control group,however,the cell migration ability and invasion ability were significantly decreased(P<0.05). Moreover the expression levels of Caspase-3 protein were obviously increased,however, the expression levels of Bcl-2 protein were significantly decreased,as compared with those in control group(P<0.05).Besides cell apoptosis was found in experimental groups,with a dose-dependent manner,as compared with that in control group(P<0.05). Conclusion AE can inhibit the proliferation of cervical carcinoma Hela cells by blocking cell cycle at G2/M phase,inducing cell apoptosis,decreasing cells' migration and invasion abilities. Moreover its action mechanism may be correlated with the upregulation of Caspase-3 protein and downregulation of Bcl-2 protein.