An experimental study on the use of icariin for improving thickness of thin endometrium.

This study aimed to investigate the effect of icariin (ICA) on thin endometrium in a rat model. To this end, 6- to 8-week-old female Sprague Dawley rats (105) were randomly divided into 7 groups: untreated, vehicle-treated (lavage with NaCl), high-dose ICA (lavage with ICA at 200 mg∙kg-1∙day-1), medium-dose ICA (lavage ICA at 100 mg∙kg-1∙day-1), low-dose ICA (lavage with ICA at 50 mg∙kg-1∙day-1), sham model (injected with NaCl at uterus horn), and sample group. To induce thin endometrium, rats of all groups (except sham-model) were injected with 95% ethanol via the uterine horn. Each group underwent its respective treatment for 3 estrous cycles, after which 5 rats from each group were sacrificed, and endometrial thickness was measured. The expression of CD31, factor VIII, vascular endothelial growth factor (VEGF), cytokeratin (CK), and vimentin were detected via immunohistochemistry. The results showed that CD31, factor VIII, and VEGF were primarily expressed in the cytoplasm of endometrial and vascular epithelial cells. No difference in the expression of these factors was detected between the ICA lavage groups and the untreated groups. However, high dose ICA-treated group exhibited significantly higher expression of CD31, factor VIII, and VEGF compared to that in the low dose and vehicle-treated groups. CK and vimentin in the endometrial tissue were significantly higher in the untreated and treatment groups compared to the vehicle-treated group. This study demonstrated that ICA increases thickness of the endometrium, and it may modulate expression of VEGF, CD31, and factor VIII.

PI3K, AKT, and P-AKT levels in thin endometrium.

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.

Effects of icariin on the expression of ER, VEGF, and KDR in the endometrial cells of thin endometrium.

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.