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¹ Section of Pathophysiology, Department of Pharmacy² Department of Health and Bio-pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, Mukogawa Women's University, Nishinomiya 663-8179, Japan³ Department of Biotics, Nichimo Company, Tokyo 140-0002, Japan⁴ Department of Surgery, Beth Israel Deaconess Medical Center at Harvard Medical School, 330 Brookline Avenue, Burlington-5, Boston, Massachusetts 02215, USA⁵ Hanabusa Women's Clinic, Kobe 650-0021, Japan⁶ Departments of Obstetrics and Gynecology, Showa University School of Medicine, Tokyo 142-8555, Japan⁷ Institute for World Health Development, Mukogawa Women's University, Nishinomiya 663-8179, Japan

(Correspondence should be addressed to J-W Xu; Email: jwxu{at}mukogawa-u.ac.jp)

Isoflavones have attracted much attention due to their association with health benefits; however, comprehensive understanding of the beneficial impacts of isoflavones on uterine biology at the molecular level remains unexplored. In the present study, our data showed that isoflavones aglycones AglyMax, genistein, and equol, but not daidzein, within the range of plasma concentration, displayed bioavailability in regulating the secretion of leukemia inhibitory factor (LIF) and transforming growth factor β (TGF-β) in Ishikawa cells, which was blocked by an estrogen receptor antagonist ICI 182 780, mitogen-activated protein kinase kinase (MEK)1/2 inhibitor PD98059, and p38 mitogen-activated protein kinase inhibitor SB203580. We also found that AglyMax and genistein increased in cyclic AMP release and the expression of glycodelin protein in Ishikawa cells assayed using western blot and immunochemical staining. The MEK1/2 inhibitor PD98059 and the protein kinase A inhibitor H89, but not SB203580, attenuated this glycoprotein expression. Moreover, isoflavone aglycones AglyMax stimulated LIF, and TGF-β secretion, and glycodelin expression in separate primary endometrial epithelial cells in the follicular phase or luteal phase from healthy subject donors. Overall, our findings suggest that isoflavones may alter the uterine expression of estrogen-responsive genes.