Objective:To investigate the proliferation inhibition effect of Arctigenin ( ARG) on endometrial carcinoma HEC-1B cell and its mechanism.Methods:HEC-1B cells were divided into test group and control group.The test group was intervened with ARG at the final concentration of 10,20,30,40,60,100 μmol/L,and the control group was intervened with 0.5%dimethyl sulfox-ide (DMSO).48 h after incubation,the proliferation was detected by MTT assay.The cell apoptosis and cell cycle were detected by flow cytometry.The expression of NF-κB signaling pathway related proteins were detected by western blotting (WB).Results:The relative survival rates of HEC-1B cell intervened with 10,20,30,40,60 and 100 mol/LARG after 48 h were (92.36 ±0.52)%, (89.59 ±0.74)%,(78.49 ±0.68)%,(56.47 ±0.59)%,(40.12 ±0.69)%,(37.52 ±0.58)%respectively,with the increase of ARG concentration.The relative survival rates of HEC-1B cells decreased gradually (P＜0.05).50% inhibitory concentration ( ID50) of HEC-1B cells intervened with ARG after 48 h was 50 μmol/L.The apoptosis rates of HEC-1B cells in the control group and the test group (50 μmol/L ARG) were (2.89 ±0.56)%,(26.58 ±3.26)%respectively.The apoptosis rate in the test group was significantly higher than that in the control group (P＜0.05).However,there was no significant difference in cell cycle distri-bution between the test group and the control group (P＞0.05).The expression levels of p65 and p-IκB-αin the test group (50 μmol/L ARG) were significantly lower than that in the control group ( P＜0.05).There was no significant difference in the ex-pression levels of IκB-αbetween the test group and the control group (P＞0.05).Conclusion:ARG can inhibit the proliferation and promote apoptosis of HEC-1B cells,and its mechanism may be related to decreasing the expression level of NF-κB related pro-tein and inhibiting the activation of NF-κB pathway.
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维普
