Objective: To apply low molecular weight heparin to treat blastocyst implantation dysfunction in mice, observe the changes of EGFR/PI3K/Akt signaling pathway, and explore its mechanism of endometrial receptivity.
Method: 72 C57BL/6 mice were randomly divided into 6 groups: blank group, model group, aspirin group, low molecular weight heparin high dose group, low molecular weight heparin medium dose group and low molecular weight heparin low dose group. used to be. Except for the blank group, other groups used indomethacin to establish blastocyst implantation dysfunction models. On the 5th day of pregnancy, the mice were sacrificed by morning cervical dislocation, and the number of transplanted uterine blastocysts was counted. Through immunohistochemistry, Western Blot and Real-detected the expression of HBEGF, EGFR, PI3K and Akt in the endometrium. Time PCR. versus
Result: Compared with the model group, the uterus of the blank group and the drug treatment group had better skin color, uniform implantation, increased number of implantation sites (P \u003cu003c0.05), and increased endometrium. The stained epithelial cells are thick, and the mesenchymal cells are relatively thick. The endometrium of each group was large and dense, with many glands and blood vessels, low molecular weight heparin and high doses of HBEGF, EGFR, PI3K, Akt protein and mRNA expression (P\u003c0. 05).
Conclusion: Low molecular weight heparin can activate the EGFR/PI3K/Akt signaling pathway by promoting the expression of HBEGF, thereby improving the receptivity of the endometrium and increasing the success rate of blastocyst implantation. I will increase it.