22 results about "Post myocardial infarction" patented technology

The invention relates to a construction method and application of a spontaneous and persistent ventricular tachycardia animal model, in particular to a spontaneous and persistent ventricular tachycardia rat model based on MYL4 gene defect and myocardial infarction induction. The model is constructed by utilizing the synergistic effect of double pathological factors of MYL4 gene conserved gene defects and acquired myocardial infarction, the induction rate of the model is greater than or equal to 90%, the spontaneous duration time reaches 1-3 min, and the method is obviously superior to an existing construction method for inducing the spontaneous and continuous ventricular tachycardia model. The model can simulate the pathophysiological process of ventricular tachycardia after human MYL4 gene related cardiovascular diseases combined with myocardial infarction, provides general technical support for ventricular arrhythmia pathogenesis research, drug screening and medical instrument research and development, and has wide scientific research and clinical transformation value.

The invention provides application of S100A4 in preparation of a medicine for promoting myocardial cell proliferation. It is found that S100A4 not only can significantly induce proliferation of newborn mouse primary myocardial cells and hiPSC-CMs in vitro, but also can significantly improve the cardiac function after myocardial infarction and relieve ventricular fibrosis through AAV9-mediated cardiac targeting overexpression in vivo, and no obvious systemic toxic or side effect or tumorigenic signs are observed. Therefore, the S100A4 protein and the means of overexpressing the S100A4 can be used for promoting myocardial cell proliferation, so that the S100A4 protein can be used for improving or treating heart injury diseases such as ischemic heart disease and the like.

The invention relates to the technical field of medicine, in particular to a brazilin-containing pharmaceutical composition and a preparation method and application thereof, and preparation raw materials comprise brazilin and a zinc preparation. Through the synergistic effect of the brazilin and the zinc preparation, the fibrosis area after myocardial infarction can be remarkably reduced, the cardiac function after myocardial infarction can be improved, and the cardiac fibrosis degree can be effectively relieved by inhibiting the expression of fibrosis-related genes and proteins at transcription and protein levels.

The invention relates to migration of CCR7-mediated dendritic cell-derived exosomes and improvement of cardiac functions after myocardial infarction, in particular to a dendritic cell-derived exosome, CCR7 expression or activity in the dendritic cell is up-regulated, CCR7 overexpression can enhance migration of the dendritic cell-derived exosomes to the spleen, and CCR7 expression or activity of the dendritic cell-derived exosomes is up-regulated. And the CCR7 knockdown weakens the migration ability of the dendritic cell source exosome.

Ischemic heart disease is a leading cause of death and reduced quality of life worldwide. Although revascularization strategies significantly reduce mortality after acute myocardial infarction (MI), many patients with MI develop chronic heart failure over time. We previously reported that human recombinant ANGPTL4 counteracts ischemia-induced vascular endothelial growth factor signaling and disruption of endothelial cell-cell adhesion, thereby inhibiting vascular permeability. We were able to demonstrate that ANGPTL4 administration before MI resulted in protection of the coronary capillary network, no-reflow syndrome, and reduced infarct size in mice. We also demonstrated that the therapeutic effects observed with ANGPTL4 under ischemic conditions were caused by the FLD fragment, not the CCD fragment (WO 2016 / 110498). To further examine the therapeutic potential of the FLD fragment of ANGPTL4 at the onset of reperfusion, we herein used a porcine model, a clinically relevant model of acute myocardial infarction that can be easily and safely translated into patient treatment. We demonstrated that local (antegrade) delivery of the FLD ANGPTL4 to infarcted porcine hearts can efficiently target the lesion site in a clinically relevant manner. A single administration of the FLD of ANGPTL4 improved cardiac function, infarct size, fibrosis, and adverse remodeling parameters 28 days after MI. Short-term MI experiments, coupled with complementary mouse studies, demonstrated myocardial protection. Thus, a single administration of the FLD of ANGPTL4 can reduce ischemia-reperfusion injury and protect against adverse postischemic cardiac remodeling and subsequent ischemic heart failure.

The invention belongs to the technical field of biological pharmacy, and provides an application of a serum LECT2 level in cardiac remodeling and coronary angiogenesis prediction after myocardial infarction, and the application is that the serum LECT2 level is used as a marker to be applied to cardiac remodeling and coronary angiogenesis prediction after myocardial infarction. By establishing a myocardial infarction animal model and comparing serum LECT2 levels in blood of healthy people, myocardial infarction patients and coronary artery occlusion patients, the prognosis effect of the serum LECT2 expression level in myocardial infarction and coronary artery occlusion diseases is evaluated. Results show that the serum LECT2 level can be used as an effective index for predicting coronary angiogenesis after myocardial infarction and prognosis of patients, and clinicians can adjust a treatment scheme in time and optimize patient management by detecting the serum LECT2 level.

The application relates to the technical field of biological medicine, and discloses medical uses of HSPD1 acetylation modification in prevention or treatment of myocardial infarction. The application first finds that the acetylation level of an HSPD1 protein K352 site is specifically up-regulated in the pathological process of myocardial infarction, and that the heart function after myocardial infarction can be significantly improved by up-regulating the acetylation level of the site, and myocardial fibrosis and myocardial cell hypertrophy can be inhibited; the acetylation level of the site is down-regulated, and myocardial ischemic injury is aggravated, and the heart function is deteriorated. The application confirms that the HSPD1 K352 site acetylation can be used as a new target point for prevention, treatment and auxiliary diagnosis of myocardial infarction, and provides a theoretical basis and experimental basis for research and development of myocardial infarction targeted drugs and gene therapy products.

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.

The invention belongs to the technical field of biological pharmacy, and provides application of American ginseng total saponins in preparation of a medicine for treating angiogenesis after myocardial infarction. Animal experiment results show that AGS can obviously improve cardiac functions of MI mice and cardiac dysfunction after myocardial infarction, and has obvious effects of improving endothelial cell functions and promoting angiogenesis. It is clear that the American ginseng total saponins may become a promising candidate drug for treating angiogenesis-related cardiovascular diseases in the future, and an effective technical means is provided for treatment of myocardial infarction.

The present invention relates to a cardiomyocyte surface-modified with a collagen-hybridized peptide and a use thereof. A cardiomyocyte surface-modified with a collagen-hybridized protein according to the present invention can have large molecules of the collagen-hybridized protein effectively inserted into the cell surface by using click chemistry, and the optimal conditions thereof were determined. In addition, it was found that the cardiomyocyte can be specifically attached to denatured collagen due to being surface-modified with the collagen-hybridized protein. In addition, it was found that, when transplanted into a myocardial infarction animal model, the cardiomyocyte increases cardiac function, attaches to areas of denatured collagen in cardiac tissue, thereby regenerating fibrotic cardiomyocytes, and inhibits cardiac remodeling, thereby providing recovery from cardiac damage after myocardial infarction.

The invention belongs to the field of biological materials and cardiovascular repair, and relates to hydrogel for repairing after myocardial infarction as well as a preparation method and application of the hydrogel. The hydrogel consists of chitosan or a derivative thereof, silk fibroin, tannic acid and a biological cross-linking agent in a weight ratio of 3: (0.8-1.2): (0.1-3.0): (0.1-0.2). According to the invention, tannic acid is introduced into the chitosan-silk fibroin composite hydrogel as a cross-linking agent and a rigidity reinforcing agent, so that the compressive strength of the hydrogel is increased from 34.4 kPa to 84.45 kPa, and the elastic modulus is increased to gt; and the mechanical property of the material is matched with that of the myocardial tissue. Meanwhile, the hydrogel can realize multi-dimensional coordinated regulation and control on oxidative stress, inflammatory response and myocardial fibrosis: in a myocardial infarction model, the hydrogel enables the left ventricular ejection fraction (LVEF) to be increased by 25%, the active oxygen clearance rate to be increased by 45%, the inflammatory cell infiltration to be reduced by 45%, the proinflammatory cytokine (IL-6 / TNF-alpha) level to be reduced by 30%, and the fibrosis area to be reduced by 40%; therefore, the heart failure process after myocardial infarction is effectively delayed.

The application discloses a kind of for preventing or treating post myocardial infarction ventricular arrhythmia pharmaceutical composition, the pharmaceutical composition is by everolimus, ethmolam and fluoxetine, belongs to the field of medicine technology.Immunoblotting proves that everolimus, ethmolam and fluoxetine can inhibit fatty acid oxidation protein.In vitro and in vitro cardiac electrophysiology experiment proves that the pharmaceutical composition can effectively reduce post myocardial infarction ventricular arrhythmia susceptibility.TTC staining proves that the pharmaceutical composition can effectively reduce post myocardial infarction myocardial damage area.Based on the above composition in the regulation of post myocardial infarction ventricular arrhythmia susceptibility, it can be further developed in the clinical application of the disease.

The invention relates to the technical field of bioinformatics and in vitro diagnosis, in particular to a prediction model, system and kit for risk assessment of acute myocardial infarction. The application systematically proves that the neutrophil-derived silk glycan (SRGN) is a key regulator of neutrophil inflammatory response in inflammatory cascade reaction after myocardial infarction, so that a model for predicting the risk of acute myocardial infarction through SRGN and neutrophil counting is determined; a corresponding kit and an evaluation system are designed according to the model. Compared with the prior art, the model and the related kit and evaluation system can quickly and accurately evaluate the risk of acute myocardial infarction in vitro.

The invention discloses application of a composition containing a tanshinone extract and muscone, and belongs to the technical field of medicines. Through compatibility and proportion control of the tanshinone extract and the musk ketone, heart fibroblast expression and / or FSTL1 secretion can be inhibited on the molecular level, related fibrosis signal channels are regulated and controlled, accordingly, the myocardial fibrosis process is inhibited, a synergistic effect with myocardial damage resistance is achieved, ventricular structure and dysfunction after myocardial infarction is improved, and the myocardial infarction treatment effect is improved. The pharmaceutical composition is used for treating cardiovascular diseases such as myocardial infarction, myocardial fibrosis and heart failure after myocardial infarction. The composition disclosed by the invention comprises tanshinone extract and muscone, and can be used for preparing medicines with better effects for preventing and treating cardiovascular diseases.

The invention relates to the field of traditional Chinese medicine, in particular to application of sophora flavescens external vesicles in preparation of a medicine for relieving myocardial fibrosis after myocardial infarction. Experiments discover that the sophora flavescens outer vesicles can significantly improve cardiac super EF and FS values of myocardial infarction mice, improve myocardial infarction areas of myocardial infarction group mice, and inhibit mRNA and protein expression levels of alpha-SMA, collagen I and collagen III, and show that the sophora flavescens outer vesicles can significantly improve cardiac dysfunction and myocardial injury caused by myocardial infarction of mice, and can significantly improve myocardial infarction of mice. Transdifferentiation and matrix collagen deposition of myocardial fibroblasts induced by TGF-beta1 are remarkably relieved, and the compound can be used for preparing drugs for relieving myocardial fibrosis after myocardial infarction and improving cardiac dysfunction and myocardial injury caused by myocardial infarction.

The invention relates to an application of a polypeptide Nod1-T9 in preparation of drugs for treating acute myocardial infarction diseases. The amino acid sequence of the polypeptide Nod1-T9 is as shown in SEQ ID NO: 1. The invention provides a bioactive polypeptide Nod1-T9 derived from a human protein Nod-1, and the polypeptide Nod1-T9 is derived from a Nod-1 key functional region, has a bioactive mechanism for regulating expression of cell inflammatory factors and resisting fibrosis, and shows excellent treatment potential in intervening cardiac remodeling and heart failure after myocardial infarction. The traditional Chinese medicine composition has anti-inflammatory and anti-fibrosis effects at the same time. The invention is derived from human body, has high safety, is derived from protein naturally existing in human body, has good immunogenicity, and has small expected toxic and side effects. The structure is stable, production is easy, the polypeptide chain is short, the structure is simple, and industrial large-scale chemical synthesis and optimization modification are facilitated.

This invention belongs to the field of biomedical materials technology and discloses an injectable hydrogel for myocardial infarction repair and its preparation method. The composite material is prepared by reacting a composite system formed from sodium alginate and gallic acid as a carrier with MXene and resveratrol, and the crosslinking agent is magnesium ions. This hydrogel exhibits excellent injectability (shear-thinning properties), biocompatibility, good conductivity, and antioxidant properties. It can be precisely delivered to the myocardial infarction lesion via minimally invasive injection, rapidly gelling after injection. It can effectively remove excess reactive oxygen species at the lesion site, reduce inflammatory response, and promote myocardial cell protection and tissue repair.

The invention discloses a novel application of a CCL1-CCR8 shaft, and relates to the technical field of biological medicines. The invention discloses for the first time that after myocardial infarction, CCL1 secreted by heart macrophages can selectively collect regulatory T cells expressing CCR8 to an injured heart and inhibit the pro-inflammatory characteristic of the macrophages, so that heart repair is driven. Based on the discovery that the CCR8 + Tregs express IL-1R2, the invention provides the following applications: an application of a preparation for promoting CCL1-CCR8 axis expression or a CCL1 / CCR8 protein in preparation of medicines for preventing and treating myocardial infarction and heart failure; the invention discloses application of a preparation for inhibiting CCL1-CCR8 axis expression in preparation of a myocardial infarction or ventricular malfunction remodeling animal model. The invention also discloses application of a preparation for detecting the expression level of CCL1 or CCR8 in preparation of a product for screening and diagnosing myocardial infarction or evaluating the prognosis of myocardial infarction. The invention provides a brand new target spot and strategy for treatment, model construction and diagnosis of myocardial infarction.

The invention discloses a pharmaceutical composition for preventing or treating ventricular arrhythmia after myocardial infarction, and belongs to the technical field of medicines. The pharmaceutical composition is prepared from everolimus, etomadectin and fluoxetine. Western blot proves that everolimus, etomadectin and fluoxetine can inhibit fatty acid oxidation protein. In-vitro and in-vitro cardiac electrophysiological experiments prove that the pharmaceutical composition can effectively reduce the ventricular arrhythmia susceptibility after myocardial infarction. TTC dyeing proves that the pharmaceutical composition can effectively reduce the myocardial injury area after myocardial infarction. Based on the regulation effect of the composition on the susceptibility of ventricular arrhythmia after myocardial infarction, the clinical application of the composition to the ventricular arrhythmia after myocardial infarction can be further developed.

The application relates to application of a MYZAP overexpression recombinant vector in preparation of a drug for preventing and treating arrhythmia, and belongs to the technical field of biological medicines. In order to solve the problem that the application of a gene drug is limited in prevention and treatment of arrhythmia after myocardial infarction, the application provides application of a myocardial zonula adherens protein MYZAP overexpression recombinant vector in preparation of a drug for preventing and treating arrhythmia, wherein the MYZAP overexpression recombinant vector is an adeno-associated virus vector AAV9-MYZAP overexpressing a MYZAP gene. In-vivo experiments prove that MYZAP overexpression can increase the MYZAP protein content in cardiac muscle cells of a heart, reduce the occurrence of arrhythmia after myocardial infarction, and improve the cardiac function and cardiac electrical conduction disturbance after myocardial infarction. Based on this, the application further provides a drug for preventing and treating arrhythmia after myocardial infarction, and provides a new strategy for gene therapy of arrhythmia after myocardial infarction, and has a wide clinical application prospect.

The present invention refers to a peptide, comprising or consisting of SEQ ID NO: 1 (CAYMTMKIRN), for use as a medicament, preferably in the prevention and / or treatment of cardiac damage arising after ischemia followed by reperfusion, or in the prevention and / or treatment of the inflammatory response following acute myocardial infarction. In a preferred embodiment, the peptide is conjugated with a nanoparticle.

This invention discloses the pharmaceutical applications of UGDH in the prevention and treatment of myocardial infarction, belonging to the field of biomedical technology. This invention is the first to demonstrate that UDP-glucose dehydrogenase (UGDH) plays a key regulatory role in the pathological process of myocardial infarction, with significantly upregulated UGDH expression in a myocardial infarction model. Fibroblast-specific knockdown of UGDH significantly improves cardiac function in mice after myocardial infarction, reduces the infarct area, and inhibits myocardial fibrosis and excessive fibroblast activation; overexpression of UGDH significantly worsens the aforementioned pathological phenotypes. This invention clarifies that UGDH can serve as a novel target for the prevention, treatment, and auxiliary diagnosis of myocardial infarction, providing a new direction for the development of gene therapy drugs for myocardial infarction.