10 results about "CD31" patented technology

The invention provides an application of a super enhancer inhibitor JQ-1 in preparation of peripheral artery disease related drugs, relates to the technical field of biomedicine, and discloses a core effect of the super enhancer inhibitor JQ-1 in peripheral artery disease ischemia repair. The traditional Chinese medicine composition can significantly accelerate blood flow recovery of ischemic limbs, up-regulate mRNA and protein expression of a vascular marker CD31 in gastrocnemius muscle tissues, effectively increase vascular density and promote angiogenesis. Aiming at the defects of the existing treatment means in the aspect of ischemic tissue angiogenesis, the application provides a brand new molecular targeted treatment scheme for high-risk groups such as patients with diabetes-related peripheral artery diseases, and can significantly reduce the risk of lower limb amputation and the incidence rate of related cardiovascular adverse events such as coronary heart disease and stroke; the technical blank of specific targeted therapy of peripheral artery diseases is filled, a solid scientific basis and a key direction are provided for research and development of novel drugs, and the specific targeted therapy method has extremely high clinical application value and wide research and development prospects.

This invention discloses a method for preparing and applying a shell-core composite flexible biomaterial. The flexible biomaterial consists of an outer PMMA electrospun layer, a middle PTFF or PE layer, and a core PEG hydrogel; both the PMMA electrospun layer and the middle layer are porous. This flexible material is soft and elastic, exhibiting good film-forming and osteogenic induction effects. Animal experiments have confirmed that, compared to traditional bone cement, the flexible composite bone cement-induced biofilm shows an increase in CD31-positive cells (representing angiogenesis) and M2 macrophages (representing tissue repair), exhibiting better film-forming properties. It is a promising composite biomaterial that can be widely applied in the treatment of soft tissue defects, bone defects, and bone infections, achieving better therapeutic effects.

The invention relates to the technical field of biological medicine and tissue engineering, in particular to a tissue engineering blood vessel and a preparation method and application thereof. The tissue engineering blood vessel is obtained by modifying interleukin 24 (IL-24) on the surface of an acellular blood vessel, after the tissue engineering blood vessel is transplanted into a body, the number of CD31 + and CD34 + cells can be remarkably increased, and infiltration of M2 type macrophages (CD163 +) on the surface of the blood vessel is remarkably increased; the expression of HIF-1 alpha (hypoxia marker) and MMP9 is obviously reduced; the expression of the nerve specific protein S-100 is obviously increased, thrombosis and intimal hyperplasia are effectively inhibited, and the patency rate of transplanted blood vessels is obviously increased.

The application discloses application of harman alkaline in preparation of a medicine for treating and / or preventing myocardial infarction; the application firstly finds that the harman alkaline can be used for treating and / or preventing myocardial infarction. Meanwhile, the harman alkaline can significantly reduce a myocardial infarction area, improve heart function, and promote blood vessel neogenesis in an infarction edge area; and the harman alkaline can also up-regulate protein expression of CD31. In a cell experiment, the harman alkaline can promote HUVEC cell migration and proliferation after H2O2 injury. The application discloses the anti-myocardial infarction effect of the harman alkaline, provides a new medicine for myocardial infarction treatment, and has important clinical application value.

This invention belongs to the field of biomedical technology, specifically disclosing an injectable embolic agent, its preparation method, and its application. The embolic agent is a hydrocolloid system containing core-shell structured nanoparticles: the core contains Cu... 2+ Salt and ATOX1 inhibitors, where ATOX1 inhibitors can inhibit copper ion efflux and promote intracellular copper accumulation, and interact with Cu 2+ It synergistically induces copper death in tumor cells; the shell is a thermosensitive block copolymer hydrogel that can interact with Cu. 2+ Coordination bonds are formed, enhancing the stability of nanoparticles, while a sol-gel transition occurs at physiological temperatures, enabling precise vascular embolization; the overall core-shell structure allows for the formation of Cu... 2+ The sustained-release effect of ATOX1 inhibitors was observed. In the VX2 rabbit hepatocellular carcinoma model, this embolization agent significantly improved tumor necrosis rate and reduced metastasis rate compared to traditional iodized oil embolization; it also downregulated hypoxia- and angiogenesis-related factors such as HIF-1α, VEGF, and CD31, inhibited MMP9-mediated tumor invasion and metastasis, and promoted CD8+. + T-cell infiltration effectively improves the tumor immunosuppressive microenvironment after transarterial chemoembolization.

The invention provides application of an NCOA3 polyQ structural domain as a target spot in preparation of a medicine for relieving lower limb ischemic diseases, relates to the technical field of biomedicine, and aims to solve the problems that in the prior art, blood flow reperfusion recovery of the lower limb ischemic diseases is poor, collateral vessels are insufficient in formation, and safe and effective targeted intervention means are lacked. By constructing a mouse lower limb ischemia model, it is proved that blood flow recovery and collateral angiogenesis after ischemia are remarkably inhibited by Nco3polyQ structural domain deletion: compared with a WT mouse, postoperative blood flow perfusion of an Nco3Q / Q mouse is recovered slowly, and the blood flow of the affected side is only recovered by 60% on the 21st day after the operation; the CD31 positive region of the gastrocnemius muscle tissue on the 14th day after the operation is obviously reduced, and the mRNA expression of the blood vessel marker gene Pecam1 is reduced. On the basis, an intervention strategy aiming at the NCOA3 polyQ structural domain is used for preparing the medicine for relieving the lower limb ischemic disease, and a new treatment strategy and a potential target are provided for the ischemic limb disease.

The application belongs to the field of biological medicine, and provides application of TGF-beta / Smad signal pathway in treatment of corneal neovascularization after corneal alkali burn. The application proves that by inhibiting the TGF-beta / Smad signal pathway, the alkali burn-induced corneal neovascularization can be significantly reduced, and the corneal pathological damage is improved, and the mechanism of action involves regulating M2 type macrophage polarization and inhibiting the process of cellular ferroptosis of corneal tissue. It is found that by using a specific inhibitor SB-431542, the expression of TGF-beta1 and p-Smad2 / 3 proteins can be effectively reduced, the angiogenic factors such as VEGFA and CD31 are reduced, the inflammatory factors such as IL-4 and IL-10 are down-regulated, the GSH level is restored, and the Fe 2+ and MDA contents are reduced. The application is suitable for developing a targeted therapeutic drug for pathological neovascularization after corneal alkali burn, and provides a theoretical basis.

The present invention relates to a culture method for culturing a population of endothelial colony-forming cells (ECFC) derived from umbilical cord blood, the method comprising: (a) holding an umbilical cord blood sample obtained from a subject at a temperature of 4 DEG C to 15 DEG C for 24 hours to 72 hours; (b) isolating mononuclear cells from the blood sample; (c) inoculating the mononuclear cells on a culture substrate; (d) culturing the inoculated adherent monocytes in a culture medium for about 5 days to about 21 days to form colonies comprising cells; and (e) culturing the cells which express the CD31, the CD34, the CD105, the CD144, the CD146, the CD157 and the VEGFR2 (vascular endothelial growth factor receptor 2) but do not express the CD45, the CD14 and the CD90.

The invention discloses application of avenanthramide D in preparation of a medicine for inhibiting angiogenesis, and relates to the technical field of biological medicine. Avenanthramide D is applied to intervene HUVEC cells, cell viability, cell apoptosis rate and angiogenesis ability after intervention are detected, and it is found that avenanthramide D can inhibit HUVEC cell proliferation, promote HUVEC cell apoptosis and inhibit HUVEC cell angiogenesis. A further experiment shows that the avenanthramide D reduces the integrity of an endothelial barrier by reducing the protein expression of a vascular endothelial growth factor A (VEGFA) and a platelet endothelial cell adhesion molecule 1 (CD31) in HUVEC cells, so that angiogenesis is blocked.

The invention provides application of an NCOA3 polyQ structural domain in preparation of a medicine for relieving ocular vascular abnormal hyperplasia diseases, relates to the technical field of biomedicine, and aims to solve the problems that in the prior art, an ocular pathological angiogenesis mechanism is complex, and safe and effective targeted intervention means are lacked. The construction of a mouse corneal micropocket pathological angiogenesis model proves that Nco3polyQ structural domain deletion can significantly inhibit corneal neovascularization: compared with a WT mouse, the Nco3wt / Q mouse corneal tissue CD31 positive signal is reduced, the number of corneal neovascularization in the Nco3Q / Q mouse is minimum, and the CD31 positive area is minimum; meanwhile, qPCR (quantitative polymerase chain reaction) detection of corneal tissues shows that mRNA (messenger ribonucleic acid) expression of the vascular marker genes Pecam1 and Cdh5 is in a decreasing trend and is further decreased in an Nco3Q / Q mouse. On the basis, the intervention strategy aiming at the NCOA3 polyQ structural domain is used for preparing the medicine for relieving the abnormal hyperplasia diseases of the ocular blood vessels, and a new treatment strategy and a potential target are provided for related diseases of the ophthalmology department.