ABSTRACT. We explored the effects of icariin on the expression of estrogen receptor (ER), vascular endothelial growth factor (VEGF), and kinase insert domain receptor (KDR) in the endometrial cells of the thin endometrium. Primary endometrial cells were obtained and divided into a blank control group, a high-, a middle-, and a low-dose icariin groups, as well as an estrogen treatment group to undergo cellular identification by immunocytochemistry. The expression levels of ER, VEGF, and its receptor were estimated by western blotting. The expression levels of ER, VEGF, and KDR gradually increased from the control group to the estrogen (E2) treatment and icariin treatment groups; the differences were statistically significant. However, the differences were not statistically significant among the different icariin dose groups. The endometrium may be thickened by icariin treatment by increasing the expression levels of ER, VEGF, and KDR in endometrial cells.

The aim of the present study was to investigate the effects of Icaritin on the proliferation and decidualization of endometrial stromal cells (ESCs). A total of 20 specimens of endometrium were collected during hysterectomy at the Gynecology Department of Shenzhen Nanshan People's Hospital (Shenzhen, China) between August 2014 and December 2015. The endometrium was digested with high concentrations of collagenase and DNase and filtered with meshes, and then the glandular epithelial and stromal cells were separated by the adhesion purification method. The purity of stromal cells was identified by vimetin and cytokeratin 7 immunostaining. The estradiol + progesterone (E2+P4) and/or cyclic adenosine monophosphate (cAMP) were added to induce an in vitro decidualization model, which was used to analyze the effect of Icaritin on the decidualization ability of the human ESCs. The decidualization markers of human ESCs, prolactin (PRL) and insulin-like growth factor-binding protein 1 (IGFBP-1), was analyzed by reverse-transcription quantitative polymerase chain reaction measurements of the mRNA levels, PRL immunostaining and ELISA analysis of the IGFBP-1 protein levels in the cells or cell culture supernatant separately. The results demonstrated that treatment with E2+P4 and/or cAMP for 96 h was able to induce decidualization in ESCs, and that the cells demonstrated polygon-shaped epithelioid changes. The cell nuclei revealed multinuclear changes, and the cells were also observed to be large and round in shape. The PRL expression and upregulated IGFBP-1 mRNA and protein levels in the E2+P4+cAMP treatment group indicated successful decidualization of the in vitro model. However, the addition of Icaritin inhibited the expression of PRL and IGFBP-1 mRNA, as well as IGFBP-1 protein in the induced ESCs compared with groups without Icaritin. These results suggest that Icaritin was able to inhibit the expression of decidualization-related genes in ESCs in vitro. However, the exact mechanisms require further investigation.

ABSTRACT. The aim of this study was to explore the expression of PI3K, AKT, and P-AKT, and to investigate the role of PI3K/AKT signaling pathway in thin endometrium. We included 40 women treated in affiliated Shenzhen Nanshan People's Hospital of Guangdong Medical University for endometrial conditions between August 2013 and January 2015, 20 with a normal endometrium, and 20 with thin endometrium. The expression of PI3K, AKT, and P-AKT was evaluated by the immunohistochemical S-P method. The expression of PI3K, AKT, and P-AKT proteins was significantly lower in the thin endometrium group than in the normal endometrium group (P < 0.05). The expression of PI3K and AKT was positively correlated with the expression of P-AKT. The expression of PI3K, AKT, and P-AKT proteins in the thin endometrium decreases during the proliferative phase, and this process could be associated with PI3K/AKT signaling.