凤香洗液对子宫内膜癌细胞的影响及机制研究OACHSSCD

Objective:To investigate the effects of Fengxiang Lotion on the proliferation,apoptosis,and autophagy of human endom-etrial cancer HEC-1B cells through the mitogen-activated protein kinase(MAPK)signaling pathway and to explore the underlying mechanisms.Methods:Fengxiang Lotion was prepared and applied to HEC-1B cells at different concentrations.Cell proliferation of HEC-1B cells was assessed using the methyl thiazolyl tetrazolium(MTT)assay.Cellular morphology was observed by 4',6-diamidi-no-2-phenylindole(DAPI)staining.Autophagy was evaluated by monodansylcadaverine(MDC)staining.Cell cycle distribution and apoptosis were analyzed by flow cytometry.Western blot analysis was performed to determine the expression levels of proteins asso-ciated with the cell cycle,autophagy,apoptosis,and the MAPK signaling pathway.Results:Fengxiang Lotion inhibited the prolifera-tion of HEC-1B cells in a concentration-and time-dependent manner.After treatment with 2 mg/mL Fengxiang Lotion for 48 h,the proportion of cells in the G0/G1 phase was decreased,whereas the proportions of cells in the S and G2/M phases were increased compared with those in the 0 mg/mL group(P＜0.01).With increasing concentrations of Fengxiang Lotion,the expression levels of the cell cycle-related proteins Cyclin A and cyclin-dependent kinase 2(CDK2)gradually decreased.Fengxiang Lotion significantly inhibited HEC-1B cell proliferation,accompanied by reduced cell volume and nuclear shrinkage.The apoptotic rate increased pro-gressively,while the expression of the anti-apoptotic protein B-cell lymphoma 2(Bcl-2)gradually decreased.In contrast,the expres-sion levels of cleaved caspase-9 and the pro-apoptotic protein Bcl-2-associated X protein(Bax)gradually increased.Fengxiang Lo-tion markedly promoted autophagy,and p62 protein expression decreased in a concentration-dependent manner.In addition,Fengx-iang Lotion significantly increased the phosphorylation levels of c-Jun N-terminal kinase(JNK)and p38.Conclusion:Fengxiang Lotion inhibits the proliferation of HEC-1B cells by suppressing the expression of CDK2 and Cyclin A,thereby inducing cell-cycle arrest.Meanwhile,it increases the phosphorylation levels of JNK and p38,activates the MAPK signaling pathway,and induces apop-tosis and autophagy.