The effect of genistein on TGF-β signal, dysregulation of apoptosis, cyclooxygenase-2 pathway, and NF-kB pathway in mice peritoneum of endometriosis model

This research aimed to investigate the effect of genistein on TGF-β, dysregulation of apoptosis, NF-κB pathway, COX-2 pathway in mice of endometriosis model. Twenty-eight female mice (Mus musculus) were divided into seven groups (n = 4), involving control (normal non-treated) group; endometriosis group; the endometriosis group treated with various genistein dosages (0.78; 1.04; 1.3 mg/day for 15 days), and endometriosis group treated with standard drug, namely leuprolide acetate (0.00975 mg each day for 15 days) or dienogest (0.0052 mg/day for 15 days). Mice of endometriosis model were made by implanting myometrial and endometrial tissues under the condition of immunodeficiency. The TGF-β, Bcl-2, Bax, NF-κB, COX-2, and PGE-2 were analyzed immunohistochemically. The increase of Bcl-2 expression in endometriosis was decreased significantly by genistein dosage of 0.78 and 1.3 mg/day (p < 0.05). The decrease of Bax expression in endometriosis was increased significantly by genistein dosage of 1.04 and 1.3 mg/day (p < 0.05). The implantation increased the expression of NF-κB, COX-2, and PGE significantly compared with the control group (p < 0.05). This increase was reduced significantly by the administration of genistein at dosage of 0.78 and 1.3 mg/day (p < 0.05). It can be concluded that genistein potentially inhibits endometriosis development through the normalization of apoptosis dysregulation, the inhibition of NF-κB and COX-2 pathways in the peritoneal tissues. Therefore, genistein can be used as a holistic treatment strategy for endometriosis.