Genistein modulates the estrogen receptor and suppresses angiogenesis and inflammation in the murine model of peritoneal endometriosis.

The purpose of this study was to investigate the effect of genistein administration on the modulation of the estrogen receptor, inhibition of inflammation and angiogenesis in the murine model of peritoneal endometriosis. A total of thirty-six mice ( Mus musculus ) were divided into six groups (n = 6), including the control group, endometriosis group, endometriosis group treated with various doses of genistein (0.78; 1.04; 1.3 mg/day), and endometriosis group treated with leuprolide acetate (0.00975 mg/day every 5 days for 15 days). Analysis of estrogen receptor-α, estrogen receptor-β, TNF-α, IL-6, VEGF, and HIF-1α were performed immunohistochemically. Expression of estrogen receptor-α, estrogen receptor-β, TNF-α, IL-6, VEGF and HIF-1α increased significantly compared with the control group ( p  < 0.05). All doses of genistein decreased the expression of estrogen receptor-α, increased estrogen receptor-β, lowered VEGF and HIF-1α significantly compared with endometriosis group ( p  > 0.05). Genistein also decreased the expression of TNF-α and IL-6 (1.04 and 1.3 mg/day) compared with the endometriosis group, reaching level comparable to that of the control group ( p  > 0.05). It was concluded that genistein is able to modulate estrogen receptor-α and estrogen receptor-β and inhibit the development of inflammation and angiogenesis in the murine model of peritoneal endometriosis. Thus, genistein can be a candidate in the treatment of endometriosis.