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Objective To explore the effect of genistein on proliferation of human endometrial endothelial cells(HEECs)and glandular epithelium.Methods In vitro HEECs and human endometrial cancer-1B cell(HEC-1B)were cultured with 0,1,10,50,100,and 200 μmol/L of genistein alone or indicated concentrations of genistein combined with 0.2 or 1 nmol/L 17β-estradiol(17β-E2).Cell proliferation was determined by[3H]-thymidine incorporation and cell cycle was measured by flow cytometry.Results After 96 hours of treatment,genistein inhibited the proliferation of HEECs in a dose-dependent manner.The stimulation index reduced from 100%(without genistein treatment)to about 1%(200 μmol/L genistein).HEECs were arrested at G1/0 and G2/M phase when treated with genistein for 96 hours.When the concentration of genistein was 200 μmol/L,the percentages of HEECs at G1/0,G2/M,and S phase were 96.0%,2.1%,and 1.9%,respectively.However,when HEECs were treated without genistein,the percentages of HEECs at G1/0,G2/M,and S phase were 76.7%,8.5%,and 14.7%,respectively.17β-E2 could not influence the effects of genistein on the proliferation of HEECs.Meanwhile,genistein could suppress the proliferation of HEC-1B.If the stimulation index of HEC-1B was defined as 100% when HEC-1B was treated with different doses of 17β-E2(without genistein),it was 67%,19%,as well as 32% when cell was supplemented with 200 μmol/L genistein combined with 0,0.2,or 1 nmol/L 17β-E2,respectively.Conclusion Genistein at the concentration of 200 μmol/L can sufficiently inhibit the proliferation of HEECs and endometrial glandular epithelium simultaneously in vitro.
Objective To explore the effect of genistein on proliferation of human endometrial endothelial cells (HEECs) and glandular epithelium. Methods In vitro HEECs and human endometrial cancer-1B cells (HEC-1B) were cultured with 0, 1, 10, 50, 100, and 200 μmol / L of genistein alone or indicated concentrations of genistein combined with 0.2 or 1 nmol / L 17β-estradiol (17β-E2). Cell proliferation was determined by [3H] -thymidine incorporation and cell cycle was measured by flow cytometry. Results After 96 hours of treatment, genistein inhibited the proliferation of HEECs in a dose-dependent manner. The stimulation index reduced from 100% (without genistein treatment) to about 1% (200 μmol / L genistein). HEECs were arrested at G1 / 0 and G2 / M phase when treated with genistein for 96 hours. When the concentration of genistein was 200 μmol / L, the percentages of HEECs at G1 / 0, G2 / M and S phase were 96.0%, 2.1%, and 1.9% respectively. Although, when HEECs were treated without genistein, the percentages of HEECs at G1 / 0, G2 / M, an d S phase were 76.7%, 8.5%, and 14.7%, respectively.17β-E2 could not influence the effects of genistein on the proliferation of HEECs. While, genistein could suppress the proliferation of HEC-1B. IF the stimulation index of HEC -1B was defined as 100% when HEC-1B was treated with different doses of 17β-E2 (without genistein), it was 67%, 19%, as well as 32% when cell was supplemented with 200 μmol / L genistein combined with 0, 0.2, or 1 nmol / L 17β-E2, respectively. Confocal Genistein at the concentration of 200 μmol / L could suffice the proliferation of HEECs and endometrial glandular epithelium simultaneously in vitro.