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 sulfoxide (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 distribution between the test group and the control group (P>0.05).The expression levels of p65 and p-IκB-α in 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 expression levels of IκB-α between 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 protein and inhibiting the activation of NF-κB pathway.