Research Article

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

Published: January 23, 2017
Genet. Mol. Res. 16(1): gmr16019126 DOI: https://doi.org/10.4238/gmr16019126
Cite this Article:
A.W. Le, Z.H. Wang, X.Y. Dai, T.H. Xiao, R. Zhuo, B.Z. Zhang, Z.L. Xiao, X.J. Fang (2017). An experimental study on the use of icariin for improving thickness of thin endometrium.. Genet. Mol. Res. 16(1): gmr16019126. https://doi.org/10.4238/gmr16019126
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Abstract

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∙day), medium-dose ICA (lavage ICA at 100 mg∙kg∙day), low-dose ICA (lavage with ICA at 50 mg∙kg∙day), 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.

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