Abstract

Objectives: This study aimed to investigate whether genistein is able to inhibit cell proliferation and expression of estrogenic receptors, and to induce apoptosis in endometriosis cells. Methods: Confluent primary endometriosis cells were divided into seven groups, including control group and genistein treatment group at doses of 5, 10, 20, 30, 40 and 50 µmol/l. The times of incubation were 6, 24 and 48 hours. Four replications are applied in each group. Expression of estrogen receptor-α and estrogen receptor-β and level of proliferation cells in cells were measured using flow cytometry. Level of apoptosis cells and Bax were measured by enzyme-linked immunosorbent technique. Results: In 6 hours of treatment, the expression of estrogen receptor-α and estrogen receptor-β significantly decreased at all doses of genistein compared with control group. The expression of estrogen receptor-α was significantly reduced in 5 until 40 µM of 24 hours genistein treatment groups in comparison to control group, but estrogen receptor-β was not significantly different. In 48 hours of treatment, the expression of estrogen receptor-α and estrogen receptor-β were significantly lower in genistein-treated groups at doses of 40 µM and 20-50 µM, respectively, compared to control group. With 6 hours of treatment, the level of KI-67 and apoptosis significantly decreased in 50 µM genistein treatment group compared to control group. The expression of KI-67 significantly reduced at all doses of 24 hours genistein treatment compared to control group. In 48 hours of treatment, the level of KI-67 and apoptosis were significantly lower in 40 µM genistein treatment group compared to control group. The level of apoptosis was significantly higher in genistein treatment group compared to control group in 24 hours 50 µM genistein treatment group. Level of Bax significantly increased in genistein treatment at the doses from 10 until 50 µM compared to that of control group. Conclusion: Genistein inhibits endometrial cell proliferation and estrogen receptor expression, and induces apoptosis in endometriosis cell culture.

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