6 results about "Endometrial Stromal Cell" patented technology

This invention discloses the application of platelet-reactive protein-4 (THBS4) in the diagnosis and treatment of endometriosis. Through bioinformatics integration analysis, clinical sample validation, and in vitro and in vivo experiments, this invention confirms that THBS4 is significantly highly expressed in both ectopic lesions and peripheral blood of patients with endometriosis, and its expression level is positively correlated with disease severity. The area under the receiver operating characteristic (AUC) curve for THBS4 alone in diagnosing endometriosis is 0.930, significantly superior to cancer antigen 125 (CA125); the AUC for the combined diagnosis of THBS4 and CA125 reaches 0.968. Simultaneously, silencing the THBS4 gene effectively inhibits the proliferation, migration, and invasion of human endometrial stromal cells, and significantly reduces the volume and fibrosis area of ​​ectopic lesions in a mouse model of endometriosis. This invention provides a highly sensitive and specific new biomarker for the non-invasive or minimally invasive early diagnosis of endometriosis, and provides new targets and candidate drugs for non-hormone-dependent targeted therapy.

The invention relates to application of arachidonic acid (ARA) in preparation of a medicine for treating sleep disorder related spontaneous abortion. Peripheral blood lipid metabolism sequencing analysis finds that the ARA content in peripheral blood serum of a patient suffering from sleep disorder and repeated pregnancy loss is most obviously reduced compared with that of a patient suffering from normal sleep and normal pregnancy; an enzyme-linked immunosorbent assay test shows that the content of ARA in decidua stromal cells (DSCs) of a patient with sleep disorder and repeated pregnancy loss is remarkably reduced compared with that of a pregnant person with normal sleep; after the endometrial stromal cells (ESCs) are subjected to ARA treatment, the in-vitro decidualization level is increased; the ARA inhibitor can be used for inhibiting the in-vitro deciduation level of the ESCs; compared with a mouse with normal sleep, the content of ARA in peripheral blood and DSCs of a mouse with sleep disorder is remarkably reduced, decidua is poor, and the abortion rate is increased; supplementing ARA can improve decidua disorder and high abortion rate caused by sleep disorder. Therefore, a potential target and a new idea are provided for diagnosis and treatment of repeated pregnancy loss related to sleep disorder.

The application belongs to the technical field of biotechnology and medicine, and specifically discloses a single-domain antibody-exosome compound (Nb-EMX2-Exos) targeting EMX2 as well as a preparation method and application thereof. The compound is prepared by covalently coupling a single-domain antibody (Nb-EMX2) specifically binding to EMX2 protein to the surface of endometrial stem cell-derived exosomes (ESC-Exos). In-vitro experiments show that the compound can specifically recognize and efficiently internalize into damaged endometrial stromal cells with high expression of EMX2, and significantly promote the migration and proliferation of the cells. In-vivo experiments further prove that the compound can precisely target and enrich in damaged endometrial tissue, effectively promote the structural repair (thicken the endometrium and reduce fibrosis) of the endometrium, and completely restore the fertility function. The application provides a novel targeted treatment preparation for solving the problems of poor targeting of natural exosomes and limited treatment effect, and has important application value in the treatment of endometrial injury repair and related infertility.

The invention provides a pharmaceutical preparation for repairing endometrial injury, and belongs to the technical field of biomedicine. The pharmaceutical preparation takes improved polypeptide as an active ingredient, and the amino acid sequence of the improved polypeptide is shown as SEQ ID NO.5. Experimental results show that the polypeptide can significantly promote proliferation and migration of human endometrial stromal cells, still maintains low cytotoxicity under high concentration, and shows excellent safety. Furthermore, in a rat endometrial mechanical injury model, the preparation can obviously increase the endometrial thickness, improve the Ki-67 positive cell rate, enhance the proliferation activity of endometrial cells and promote the repair of damaged tissues. Compared with the original polypeptide, the preparation disclosed by the invention shows unexpected technical effects in the aspects of repairing activity and safety, and has a good application prospect.

This disclosure belongs to the field of pharmaceutical technology, and specifically relates to the application of targeted proline metabolic enzymes in the treatment of endometriosis. This disclosure, through in vitro experiments and EMS animal models, verifies that the proline content in ectopic endometrial stromal cells increases, the expression of proline synthesis metabolic enzymes is elevated, and fibrosis is significantly activated. This disclosure creatively repurposes proline metabolic enzyme inhibitors for EMS treatment. Proline metabolic enzyme inhibitors specifically inhibit the enzyme activity of key proline metabolism enzymes, blocking the synthesis pathway from glutamate to proline, and directly reducing intracellular proline content. Since proline is a major component amino acid of collagen, the inhibition of proline synthesis directly inhibits collagen synthesis and the expression of fibrosis markers in endometrial stromal cells, ultimately achieving the therapeutic effect of inhibiting fibrosis in EMS ectopic lesions and reducing ectopic lesion growth.

The application discloses application of miR-2355-3p in endometriosis, and finds that the RNA transcription level of miR-2355-3p in ectopic endometrial tissue samples is significantly decreased for the first time; the mimics RNA of miR-2355-3p overexpression is cloned to a lentivirus vector and lentivirus packaging is carried out, miR-2355-3p mimic lentivirus is obtained, and ectopic endometrial stromal cells are transfected with the lentivirus, so that the proliferation of the ectopic endometrial stromal cells can be inhibited, and apoptosis of the ectopic endometrial stromal cells can be promoted, thereby the growth of ectopic endometrial tissue is inhibited, and a new possibility is provided for development of an endometriosis treatment drug.