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P-224 Research on the Molecular Mechanism of rhG - CSF Affecting Embryonic Adhesion

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Abstract Study question Can rhG - CSF increase the embryo adhesion rate? Summary answer rhG - CSF can promote embryo adhesion. What is known already rhG - CSF is a glycoprotein that mainly acts on neutrophils to promote their proliferation, differentiation, and activation. Currently, rhG - CSF is commonly used in the adjuvant treatment of cancer chemotherapy and in the treatment of hematological diseases.Studies have shown that a lack of rhG - CSF may lead to recurrent miscarriage, indicating that rhG - CSF plays a regulatory role in ovulation, endometrial receptivity regulation, and the embryo implantation process.Previous research by our group has demonstrated that rhG - CSF ultimately affects the embryo implantation rate in patients with RIF by down - regulating the expression of hsa_circ_0001550. Study design, size, duration Combining in - vitro and in - vivo experiments, we evaluated the effect of rhG - CSF on embryo adhesion. In vitro, Ishikawa cells were treated with rhG - CSF for 24 h and a BeWo - Ishikawa adhesion model was used. In vivo, a mouse endometrial injury model was built, rhG - CSF was infused, then uterine tissues were tested. Fertility was assessed by counting implantation sites. Participants/materials, setting, methods Treat both normal and hsa_circ_0001550 overexpressing Ishikawa cells and hESCs with 0.5 ng/ml rhG - CSF. Establish a mouse model of endometrial injury and assign it into control, model, and rhG - CSF treatment groups.Compare the expressions of endometrial receptivity markers.Measure the embryo adhesion rate after 24 - hour treatment with 0.5 ng/ml rhG - CSF in an in - vitro embryo adhesion model and analyze the embryo implantation rate in mice from each group. Main results and the role of chance (1) Compared with the control group, rhG - CSF significantly increased the embryo adhesion rate. (2) Gene expression analysis showed that the expression of molecules related to endometrial receptivity was up - regulated after rhG - CSF treatment. (3) Immunofluorescence studies confirmed a higher degree of MET in the rhG - CSF treatment group. (4) Fertility studies confirmed that rhG - CSF could increase the number of implantation sites in the damaged endometrium and improve fertility. The results of this study indicate that rhG - CSF can promote embryo adhesion. Limitations, reasons for caution The detailed signaling pathways involved in the effect of rhG - CSF on embryo implantation in this process need further study. Wider implications of the findings These research results provide a new perspective on the factors affecting embryo implantation and have potential application value in improving the success rate of assisted reproductive technologies. Trial registration number No
Title: P-224 Research on the Molecular Mechanism of rhG - CSF Affecting Embryonic Adhesion
Description:
Abstract Study question Can rhG - CSF increase the embryo adhesion rate? Summary answer rhG - CSF can promote embryo adhesion.
What is known already rhG - CSF is a glycoprotein that mainly acts on neutrophils to promote their proliferation, differentiation, and activation.
Currently, rhG - CSF is commonly used in the adjuvant treatment of cancer chemotherapy and in the treatment of hematological diseases.
Studies have shown that a lack of rhG - CSF may lead to recurrent miscarriage, indicating that rhG - CSF plays a regulatory role in ovulation, endometrial receptivity regulation, and the embryo implantation process.
Previous research by our group has demonstrated that rhG - CSF ultimately affects the embryo implantation rate in patients with RIF by down - regulating the expression of hsa_circ_0001550.
Study design, size, duration Combining in - vitro and in - vivo experiments, we evaluated the effect of rhG - CSF on embryo adhesion.
In vitro, Ishikawa cells were treated with rhG - CSF for 24 h and a BeWo - Ishikawa adhesion model was used.
In vivo, a mouse endometrial injury model was built, rhG - CSF was infused, then uterine tissues were tested.
Fertility was assessed by counting implantation sites.
Participants/materials, setting, methods Treat both normal and hsa_circ_0001550 overexpressing Ishikawa cells and hESCs with 0.
5 ng/ml rhG - CSF.
Establish a mouse model of endometrial injury and assign it into control, model, and rhG - CSF treatment groups.
Compare the expressions of endometrial receptivity markers.
Measure the embryo adhesion rate after 24 - hour treatment with 0.
5 ng/ml rhG - CSF in an in - vitro embryo adhesion model and analyze the embryo implantation rate in mice from each group.
Main results and the role of chance (1) Compared with the control group, rhG - CSF significantly increased the embryo adhesion rate.
(2) Gene expression analysis showed that the expression of molecules related to endometrial receptivity was up - regulated after rhG - CSF treatment.
(3) Immunofluorescence studies confirmed a higher degree of MET in the rhG - CSF treatment group.
(4) Fertility studies confirmed that rhG - CSF could increase the number of implantation sites in the damaged endometrium and improve fertility.
The results of this study indicate that rhG - CSF can promote embryo adhesion.
Limitations, reasons for caution The detailed signaling pathways involved in the effect of rhG - CSF on embryo implantation in this process need further study.
Wider implications of the findings These research results provide a new perspective on the factors affecting embryo implantation and have potential application value in improving the success rate of assisted reproductive technologies.
Trial registration number No.

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