511 results about "Myocyte" patented technology

The invention discloses application of an RNF130 activator in preparation of a medicine for preventing and / or treating ischemic heart disease, and belongs to the technical field of biological medicine. Research results show that when an RNF130 activator is given in a mouse of a myocardial ischemia reperfusion injury model, the left ventricular ejection fraction and the left ventricular short-axis shortening rate of the mouse can be improved, myocardial tissue pathological injury can be relieved, the protein expression levels of NOX-2, BAX and TNF-alpha are reduced, the myocardial infarction area is reduced, and myocardial cell apoptosis is reduced; therefore, the RNF130 activator has prevention and treatment effects on the myocardial ischemia-reperfusion injury, that is, the RNF130 activator can be used as an effective component of the medicine for preventing or treating diabetes complicated by myocardial ischemia-reperfusion injury, and a new strategy is provided for preparation of the medicine for preventing and treating myocardial ischemia-reperfusion injury.

The invention discloses a bionic nano-composite, a preparation method thereof and application of the bionic nano-composite in preparation of a product for treating atherosclerosis, and belongs to the technical field of medicine preparation. The bionic nano compound is a metal nano enzyme Ir-TiO2 coated by an M2 macrophage cell membrane. According to the invention, the surfaces of Ir-TiO2 nanoparticles are coated with M2 macrophage membranes, so that the nanocomposite with a bionic structure is prepared. After intravenous injection, the formed bionic nanocomposite can actively target endothelial cells in atherosclerotic lesions, and release Ir-TiO2 antagonism to endothelial cells in plaques and cytoplasm of inflammatory macrophages. After the Ir-TiO2 reaches the diseased region, the Ir-TiO2 can play an enzyme role to achieve an anti-inflammatory effect, and can promote inflammatory cells such as macrophages and smooth muscle cells at the diseased region to discharge cholesterol, reduce lipid deposition in the cells, reduce the generation of foam cells and promote the growth of plaques. The nanotherapy can effectively prevent the progress of atherosclerosis lesion inflammation and relieve atherosclerosis.

The invention belongs to the technical field of biological medicines, and particularly relates to application of oxibenzophenone in preparation of a medicine for treating pathological cardiac hypertrophy and / or heart failure. Research results in myocardial cells of primary newborn rats show that Exibenzophenone can inhibit pathological hypertrophy of myocardial cells induced by phenylephrine (PE). Animal experiments show that the epoxybenzophenone can improve cardiac dysfunction induced by aortic arch constriction (TAC) and reduce cardiac hypertrophy and cardiac tissue fibrosis. The invention provides a new drug research and development approach and a drug action target for treating pathological cardiac hypertrophy and heart failure, and has very important medicinal value.

The invention discloses a stem cell exosome based on targeted fusion polypeptide modification, a preparation method and application of the stem cell exosome in treating male erectile dysfunction. According to the exosome, a specific targeting fusion polypeptide (sequence: EPLQLKM-GGGS-DPPV) is anchored on the surface through a chemical coupling technology, so that the targeting property of the exosome on cavernosum smooth muscle cells is enhanced; meanwhile, an anti-TrkA monoclonal antibody (TrkA-2E7-HL) is loaded through an electroporation method, and a fibrosis pathway mediated by a nerve growth factor (NGF) is inhibited. The exosome induces secretion of the umbilical cord mesenchymal stem cells by adopting an anti-oxidation culture medium, so that the anti-oxidation activity of the exosome is remarkably improved. Experiments show that in a diabetes ED rat model, the erectile function (ICP / MAP ratio) of the modified exosome is improved to 0.79 + / -0.05, the fibrosis area is reduced to 9.2 + / -1.6%, and the NO secretion level is improved by 3.5 times compared with that of a common exosome. Through triple mechanisms of polypeptide targeting, antibody synergy and oxidation resistance, effective reversion of the ED pathological process is realized, and the polypeptide has remarkable novelty and clinical transformation potential.

The invention provides a uterine muscle cell tension analysis method based on a uterine muscle cell activity image, and relates to the technical field of image processing. The method comprises the steps of tension analysis mode obtaining, resting state analysis mode tension analysis, uterine contraction state analysis mode tension analysis and tension analysis result feedback. According to the method, a tension analysis mode is obtained, if the tension analysis mode is a resting state analysis mode, a resting uterine muscle cell image is obtained, and a resting uterine muscle cell tension analysis result is obtained, and if the tension analysis mode is a uterine contraction state analysis mode, a uterine contraction uterine muscle cell image is obtained, and a uterine contraction uterine muscle cell tension analysis result is obtained. Finally, the uterine muscle cell tension analysis result is transmitted to a preset medical staff terminal, the reliability of the uterine muscle cell tension analysis result is improved, and the problem that in the prior art, the reliability of the uterine muscle cell tension analysis result is unstable due to the difference of ultrasonic probe scanning is solved.

The invention discloses a preparation method and application of a response type NO release anticoagulant hydrogel material. The preparation method comprises the following steps: providing methylacryloylated recombinant collagen; providing methacrylated hyaluronic acid; providing caffeic acid arginine amide modified hyaluronic acid; the response type NO release anticoagulant hydrogel material is obtained by taking methylacryloylated recombinant collagen, methylacryloylated hyaluronic acid and caffeic acid arginine amide modified hyaluronic acid as raw materials. The prepared hydrogel material has the advantages of resisting bacteria, promoting proliferation of endothelial cells, inhibiting proliferation of smooth muscle cells, resisting inflammation, promoting angiogenesis, inhibiting thrombosis and the like, arginine can serve as an endogenous NO donor in blood to release NO molecules, and therefore the effect of promoting vascular endothelial repair is achieved, and the hydrogel material has the advantages of being capable of resisting bacteria, promoting proliferation of endothelial cells, inhibiting proliferation of smooth muscle cells, resisting inflammation, promoting angiogenesis, inhibiting thrombosis and the like. The introduced NO molecules enable the hydrogel material to have good anticoagulant performance, and the hydrogel material is expected to be used for preparing an artificial blood vessel anticoagulant coating.

The invention provides a dilated cardiomyopathy zebrafish model and a construction method and application thereof, and belongs to the technical field of biology.The dilated cardiomyopathy zebrafish model is constructed by overexpressing miR-16-5p in myocardial cells of zebrafish, and the sequence of miR-16-5p is shown as SEQ ID NO.1; the invention further provides a construction method of the dilated cardiomyopathy zebra fish model. The invention constructs the dilated cardiomyopathy zebrafish model of overexpression miR-16-5p in myocardial cells for the first time, and the dilated cardiomyopathy zebrafish model can be used for screening drugs for resisting dilated cardiomyopathy.

The invention relates to application of an MYZAP overexpression recombinant vector in preparation of a medicine for preventing and treating arrhythmia, and belongs to the technical field of biological medicines. In order to solve the problem that application of gene drugs in prevention and treatment of arrhythmia after myocardial infarction is limited, the invention provides application of a myocardial microbelt adhesion protein MYZAP overexpression recombinant vector in preparation of drugs for prevention and treatment of arrhythmia, and the MYZAP overexpression recombinant vector is an adeno-associated virus vector AAV9-MYZAP of an overexpression MYZAP gene. In-vivo experiments prove that MYZAP overexpression can reduce the occurrence of arrhythmia after myocardial infarction by increasing the content of MYZAP protein in cardiac myocardial cells, and improve cardiac functions and cardiac electrical conduction disorders after myocardial infarction. On the basis, the invention further provides a medicine for preventing and treating arrhythmia after myocardial infarction, a new strategy is provided for gene therapy of arrhythmia after myocardial infarction, and the medicine has a wide clinical application prospect.

Disclosed in the present invention is a use of alisol-B23-acetate (AB23a) in the preparation of a drug for preventing or treating hypertrophic cardiomyopathy and diseases caused by the hypertrophic cardiomyopathy. The present invention provides for the first time a use of AB23a in the prevention or treatment of hypertrophic cardiomyopathy. According to the present invention, use of AB23a in direct in vitro treatment of cardiomyocytes derived from directed differentiation of human embryonic stem cells revealed that AB23a-based in-vitro treatment can significantly inhibit hypertrophic phenotypes of the human embryonic stem cells-cardiomyocytes; using an AB23a-containing feed to feed mice with hereditary hypertrophic cardiomyopathy caused by a gene mutation revealed that AB23a prominently relieves pathological myocardial hypertrophy of the mice and improves the cardiac function; AB23a can be used for preparing a drug for resisting hereditary hypertrophic cardiomyopathy, offering a novel way and means for treating hypertrophic cardiomyopathy; and AB23a is the main medicinal ingredient in the traditional Chinese medicinal herb-Rhizoma Alismatis, is safe to organisms, and has good clinical application prospects.

The invention provides a method for producing cell culture meat through 3D scaffold-free co-culture of pseudosciaena crocea stem cell spheres, and belongs to the technical field of preparation of cell culture meat. A method for producing cell culture meat by 3D scaffold-free co-culture of pseudosciaena crocea stem cell spheres comprises the following steps: mixing and inoculating pseudosciaena crocea myoblasts and pseudosciaena crocea precursor adipocytes into a cell culture plate subjected to anti-adhesion treatment for proliferation culture, spontaneously gathering to form cell spheres, and carrying out differentiation culture to obtain the cell culture meat. According to the co-culture mode provided by the invention, high-efficiency myogenic differentiation and adipogenic differentiation of myoblasts and precursor adipocytes of the large yellow croakers can be realized through proliferation culture and differentiation culture, and an in-vivo microenvironment can be effectively simulated, so that cultured meat similar to a traditional meat product in texture and flavor is produced.

The present invention pertains to a polypeptide comprising the amino acid sequence according to SEQ ID NO: 1 or a variant or fragment thereof for use in treating or preventing heart failure, myocardial infarction or hypertrophy, reducing infarct size or scar size after myocardial infarction, inducing endothelial cell sprouting after myocardial infarction, protecting cells from ischemia- or reperfusion-induced injury, promoting angiogenesis after myocardial infarction, promoting coronary endothelial cell migration and proliferation, inhibiting cardiomyocyte hypertrophy, or inhibiting inflammation. The present invention further provides a nucleic acid sequence encoding the polypeptide, vectors comprising the nucleic acid sequence, host cells comprising the nucleic acid or vector, and respective pharmaceutical compositions for the same use.

Described herein are targeting moieties that can be capable of specifically targeting muscle cells and can include an n-mer motif. In some embodiments, the n-mer motif contains an RGD motif. Also described herein are vector systems, particles, polypeptides that can encode and / or contain one or more targeting moieties. Also described herein are methods of delivering a cargo to a cell, such as a muscle cell, using one or more of the targeting moieties described herein.

The invention provides a construction method and application of a dilated cardiomyopathy animal model, belongs to the technical field of biological medicine and animal genetic model construction, and provides a novel dilated cardiomyopathy zebrafish model which is constructed by specifically overexpressing a truncated dnajb6b gene long isomer fragment in zebrafish myocardial cells. The nucleotide sequence of the gene segment is as shown in SEQ ID NO. 1; the invention also provides a construction method and application of the dilated cardiomyopathy zebra fish model, and further discovers application of 4-phenylbutyric acid in preparation of drugs for treating dilated cardiomyopathy.

The invention relates to the field of biomedicine, in particular to application of PXDC1 in preparation of a product for treating myocardial hypertrophy. The invention discloses the effectiveness of inhibiting PXDC1 expression in treating cardiac hypertrophy and controlling the occurrence and development process of the cardiac hypertrophy for the first time. The invention provides a novel drug target and strategy for treating myocardial hypertrophy, and the novel drug target and strategy can reduce the expression of a myocardial hypertrophy biomarker, reduce the size of myocardial cells, improve the ejection fraction and short axis shortening rate of the heart, reduce the weight ratio of the heart and relieve the degree of myocardial fibrosis. Besides, the invention clarifies the action mechanism of PXDC1 in myocardial hypertrophy, deepens the understanding of the pathogenesis of the disease, and lays an important foundation for further exploration of myocardial hypertrophy-related cytobiology and molecular biology processes.

To provide treatment of arrythmia caused by taking of myocardial cells derived from stem cell in methods for treating heart failure.SOLUTION: The invention relates to an antiarrhythmic agent, an antiarrhythmic myocardial cell population, a method for obtaining an antiarrhythmic myocardial cell population by in vitro exposure of stem cell-derived myocardial cells to an antiarrhythmic agent, and / or medical use of antiarrhythmic myocardial cell population in the prevention of arrythmia and in the treatment of heart failure.SELECTED DRAWING: None

The invention provides a hypertrophic cardiomyopathy zebrafish model and a construction method and application thereof, and belongs to the technical field of biology, the hypertrophic cardiomyopathy zebrafish model is constructed by overexpressing miR-29a in myocardial cells of zebrafish, and the sequence of the miR-29a is shown as SEQ ID NO.1; the invention further provides a construction method of the hypertrophic cardiomyopathy zebra fish model. The hypertrophic cardiomyopathy zebrafish model Tg (cmlc2: miR-29a, EGFP) with overexpression of miR-29a in myocardial cells is constructed for the first time, and the hypertrophic cardiomyopathy zebrafish model Tg (cmlc2: miR-29a, EGFP) can be used for screening drugs for resisting hypertrophic cardiomyopathy.

The invention relates to application of piRNA-AB352916 and a mimetic thereof in preparation of a medicine for treating ischemic heart disease, and belongs to the technical field of medicines. In order to solve the problem that a medicine capable of promoting myocardial cell proliferation and inhibiting myocardial cell apoptosis is lacked in the treatment process of the ischemic heart disease, the invention provides application of piRNA-AB352916 and a mimetic thereof in preparation of a medicine for treating the ischemic heart disease. According to the application disclosed by the invention, the expression level of the piRNA-AB352916 in myocardial regeneration model tissues after cardiac apex resection is obviously increased, and animal experiments prove that the myocardial specific overexpression piRNA-AB352916 not only can promote myocardial cell proliferation, but also can inhibit myocardial cell apoptosis, so that the myocardial infarction area is reduced, and the cardiac function of an infarction mouse is improved. The invention proves that the piRNA-AB352916 and the analogue thereof have prevention and treatment values on the ischemic heart disease.

The invention discloses shRNA (short hairpin Ribonucleic Acid) for targeted knockout of an Eif2ak2 gene and application, and belongs to the technical field of gene engineering. The shRNA comprises a positive-sense strand and an antisense strand which is reversely complementary with the positive-sense strand, and the nucleotide sequence of the positive-sense strand is shown as SEQ ID NO. 5. It is found for the first time that the recombinant adeno-associated virus capable of inhibiting Eif2ak2 gene expression can successfully inhibit the phenotype of the abdominal aortic aneurysm of a mouse, obviously reduce the morbidity of the abdominal aortic aneurysm of the mouse, improve the severity of the abdominal aortic aneurysm of the mouse, reduce the inner diameter of a blood vessel and the ratio of the weight to the body weight of the blood vessel, and promote the contraction function of vascular smooth muscle cells of the mouse; the method can be used for effectively treating the abdominal aortic aneurysm, provides a new thought and strategy for treating the abdominal aortic aneurysm, and has a wide clinical application prospect.

The invention discloses application of a JMJD6-targeted reagent in preparation of a medicine for promoting myocardial cell proliferation. The medicine can promote myocardial cell proliferation after myocardial infarction and reduce the myocardial fibrosis scar area caused by myocardial infarction. AAV9 myocardial specific overexpression virus and JMJD6 myocardial specific knockout mice are utilized, and the positive effect of JMJD6 in promotion of P1 cardiac apex resection of newborn mice and regeneration and repair of injured hearts after myocardial infarction of adult mice is disclosed for the first time; the specific mechanism is that JMJD6 depends on the activity of histone demethylase, enrichment of active modification H4R3me2a and H3R2me2s in a PDK4 promoter region is removed, transcriptional expression of the H4R3me2a and the H3R2me2s is inhibited, an impaired heart energy substrate utilization mode is stimulated to be increased and converted from fatty acid oxidation energy supply to glycolysis oxidation energy supply, and then adult myocardial cell proliferation is effectively promoted. The regeneration and repair capability of the heart after myocardial infarction is greatly improved, and a new effective target spot is provided for clinical treatment of myocardial injury.

The invention provides application of alpha-ketobutyrate in preparation of drugs for prevention and / or treatment of skeletal muscle atrophy, and belongs to the technical field of biomedicine.The human endogenous metabolite alpha-ketobutyrate is applied to prevention and treatment of skeletal muscle atrophy, the side effect is small, the safety is high after long-term use, and the effect is obvious. Serious immunoreaction or toxic reaction can be avoided, and skeletal muscle senescence and muscular atrophy can be effectively prevented and treated. The alpha-ketobutyrate can improve the muscle index of skeletal muscles of the old mice, increase the number of muscle fibers, increase the cross sectional area, increase the number of muscle cell nucleuses and the expression of nuclear fiber layer protein LamB1 of the muscle cell nucleuses, and can also increase the capillary angiogenesis rate in muscle tissues of the old mice. Alpha-ketobutyrate has good pharmacological characteristics and low side effects, and provides an important basis for developing clinical drugs for treating amyotrophy.

The present invention provides an extract having excellent anti-obesity and muscle cell loss prevention effects, and a single compound obtained therefrom. A pharmaceutical composition for preventing and treating muscle loss and anti-obesity, comprising an extract of Rhododendron mucronulatum as an active ingredient, is provided.

The invention relates to the technical field of biological medicines, and discloses application of AVEN as a target spot in preparation of a medicine for treating adriamycin cardiomyopathy. Wherein the AVEN is taken as the target spot, the AVEN is overexpressed by targeting cardiac myocardial cells, and further, the overexpressed AVEN by targeting cardiac myocardial cells comprises the step of improving the expression of the AVEN gene in the cardiac myocardial cells by adopting a substance capable of activating or up-regulating the expression of the AVEN in a targeting manner. It is found for the first time that specific overexpression of AVEN in myocardial cells can inhibit ferroptosis of myocardial cells, relieve myocardial fibrosis and myocardial atrophy, significantly improve adriamycin-induced cardiac dysfunction, and improve life quality and long-term prognosis of patients.

The present invention relates to a method for preparing cardiac organoids derived from human pluripotent stem cells, and an efficacy and toxicity evaluation technique. When the cardiomyocytes and cardiac organoids purified by a CD47 surface marker, of the present invention, are used, mature cardiomyocytes and cardiac organoids can be formed, and the cardiomyocytes and cardiac organoids are characterized in that mature cardiomyocytes having uniform contractile ability and a large surface area are formed at a high rate, and thus the present invention can be effectively used in cardiovascular disease modeling including that in toxicity evaluation and drug screening.

The technology disclosed herein relates to compositions and methods for improving the electrophysiological maturity of in vitro-differentiated cardiomyocytes. Media that promote electrophysiological maturation are described, as well as methods for the use of such media and the electrophysiologically matured cardiomyocytes in e.g., transplant and regenerative medicine procedures. The technology described herein is directed to cardiomyocyte maturation medium. Also described herein are associated compositions, kits, and matured cardiomyocytes. The cardiomyocyte maturation medium disclosed here can be used to modulate at least one electrophysiologic property of a cardiomyocyte. The electrophysiologically matured cardiomyocytes can engraft into cardiac tissue and can reduce or inhibit engraftment arrythmia in a subject.

The invention provides a fish precursor fat cell myogenic differentiation and pluripotent differentiation culture medium, a method for inducing myogenic differentiation and pluripotent differentiation and application, and particularly belongs to the technical field of cell biology. The differentiation culture medium for inducing the fish precursor fat cells to differentiate into the muscle cells comprises a myogenic differentiation culture medium and a differentiation maintenance culture medium. According to the myogenic differentiation culture medium, the large yellow croaker precursor fat cells can be induced to be differentiated towards muscle cells through the regulation and control effect of growth factors, and the differentiation maintaining culture medium can maintain myogenic differentiation and enhance the quality of myotubes; by combining the adipogenic differentiation culture medium, the directional pluripotent differentiation of the precursor adipocytes to different types of cells can be finally realized, and myotubes and adipocytes are efficiently formed. The preparation of the cell culture meat provides a new strategy and method.

The invention discloses an effect and application of RNA (Ribonucleic Acid) binding protein in skeletal muscle injury repair, and relates to the technical field of new application of medicines. A large number of experiments show that the RNA binding protein ARPP21 is up-regulated in the repair process after skeletal muscle injury. After the ARPP21 is knocked out, the repair capability of the mouse after skeletal muscle injury is weakened, and myoblast differentiation is inhibited. And when the ARPP21 is over-expressed, early migration of mouse myoblast differentiation can be promoted. Therefore, the ARPP21 plays an important regulating role in regeneration and repair after the skeletal muscle injury, can be used for preparing a medicine for regeneration and repair after the skeletal muscle injury, and provides a new clue and strategy for rehabilitation treatment after the skeletal muscle injury.

The invention discloses application of sulfhydrylated hyaluronic acid or salt thereof in myocardial ischemia-reperfusion injury, and belongs to the technical field of biomedical treatment. In the application, the substitution degree of sulfydryl of the synthesized sulfhydrylated hyaluronic acid or salt thereof can reach 10-40%. The oxidation resistance of 5mg / ml of sulfhydrylated hyaluronic acid or salt thereof can reach more than 50%; in the SI / RI model of the H9C2 myocardial cells, the HA-SH can protect the H9C2 myocardial cells, and meanwhile, the oxidative stress injury in the SI / RI model can be remarkably reduced; in a constructed rat myocardial ischemia reperfusion injury model, HA-SH can relieve oxidative stress injury, cell apoptosis and inflammatory response caused by myocardial ischemia reperfusion by regulating and controlling an Nrf2 signal channel and an HO-1 signal channel, reduce the iron death rate and play a role in protecting the heart. The invention provides a new drug research and development approach, and has important significance in the technical field of biomedical treatment.

The invention provides application of a DDX3X inhibitor in preparation of a medicine for treating myocardial fibrosis, and relates to the technical field of biological medicines. The invention relates to an application of a DDX3X inhibitor in preparation of a medicine for treating myocardial fibrosis. The invention proves that the myocardial cell fibrosis can be inhibited after the DDX3X is knocked down or knocked out, and the DDX3X inhibitor can interfere with the occurrence and development of mouse cardiac fibrosis and improve the cardiac function, thereby prompting that the DDX3X serving as the target of the anti-fibrosis medicine has a good medical transformation prospect, and further providing a research basis for preparing the anti-cardiac fibrosis medicine.

The invention relates to the field of biological medicine, and discloses application of inosine in preparation of a myocardial cell ferroptosis inhibitor. The invention discloses that inosine has the function of inhibiting myocardial ferroptosis for the first time, so that a new drug is expected to be developed for targeting myocardial ferroptosis, and a new theoretical basis and a potential intervention strategy are provided for myocardial injury repair.

The invention discloses an application of a traditional Chinese medicine monomer hypericin in preparation of related medicines for improving mitochondrial energy metabolism disorder and controlling oxidative stress to prevent and treat ischemic heart disease. The invention provides an application of hypericin in preparation of a product for improving mitochondrial energy metabolism disorder. The mitochondrial energy metabolism disorder is caused by myocardial ischemia reperfusion injury. Researches show that the hypericin regulates energy metabolism and oxidative stress of mitochondria by up-regulating / activating an AMPK / PGC-1alpha signal channel, so that myocardial cell apoptosis is relieved, and finally the protection effect on myocardial ischemia-reperfusion injury is achieved. The invention provides a new thought and a new method for treating MIRI by traditional Chinese medicines.