74 results about "Post myocardial infarction" patented technology

The invention relates to hydrogel loaded with oxygen self-producing nanoparticles as well as a preparation method and application of the hydrogel. The preparation method comprises the following steps: 1, taking cross-linked methacrylamide silk fibroin and hyaluronic acid modified by arginine-glycine-aspartic acid peptide as base materials, and loading self-oxygen-producing nano particles CaO2 (at) PVP (at) Cu-EGCG, and the self-oxygen-producing nano particles CaO2 (at) PVP (at) Cu-EGCG are prepared by coating Cu-EGCG on calcium peroxide nano particles modified by PVP modified polyvinylpyrrolidone. The hydrogel can improve energy metabolism and regulate immune environment through dual mechanisms, realizes efficient promotion of myocardial repair, and provides a new strategy and thought for tissue regeneration and functional recovery after myocardial infarction.

The invention belongs to the field of compositions of biomedical materials and high-molecular compounds, and provides hydrogel capable of regulating and controlling the redox steady state of a microenvironment as well as a preparation method and application of the hydrogel. A macromolecular network of the hydrogel capable of regulating and controlling the redox steady state of the microenvironment is formed by catechol modified hyaluronic acid, carboxylated chitosan, oxidized dextran and iron ions through a hybridization cross-linking reaction; under physiological conditions, catechol groups in the hydrogel can be subjected to an autoxidation reaction to generate H2O2, and meanwhile, iron ions coordinated on the catechol groups in the hydrogel can catalytically decompose H2O2 into water and oxygen, so that the level of active oxygen in a microenvironment is adjusted. The hydrogel disclosed by the invention can realize bidirectional regulation and control on active oxygen in a pathological microenvironment after myocardial infarction, so that the redox steady state of the pathological microenvironment after myocardial infarction is maintained, and the regeneration and repair capacity of an existing hydrogel material with antioxidant capacity on myocardial tissues after myocardial infarction is improved.

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.

The invention discloses application of nano-iron in vascular endothelial cells, and belongs to the technical field of cell engineering and genetic engineering. According to the invention, PEI coated Fe3O4 is taken as a research object, the application of PEI coated Fe3O4 in vascular endothelial cells is researched by adopting a molecular and cell biology method, and regulation of PEI coated Fe3O4 on vascular endothelial regeneration of the vascular endothelial cells after myocardial infarction is verified from multiple levels and multiple angles. The invention can provide a new reference for the recovery of cardiac functions after myocardial infarction, and has good application value.

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 a self-adaptive multifunctional hydrogel system for cardiac microenvironment regulation after myocardial infarction as well as a preparation method and application of the self-adaptive multifunctional hydrogel system, and belongs to the technical field of biomedical materials. The hydrogel system is hydrogel prepared by taking a micromolecular cross-linking agent, a polymer matrix and drug-loaded microspheres as raw materials. The hydrogel can realize staged response drug release in oxidative stress, inflammation and fibrosis microenvironments after myocardial infarction, has good injectability and self-healing property, and has the functions of ROS removal, nitric oxide release and the like. The invention provides a new strategy for tissue repair after myocardial infarction with multi-channel collaboration and accurate pathological response control.

The invention provides an SLC25A4 gene as well as an interferent and application thereof, and relates to the technical field of biomedicine. The SLC25A4 gene interferent is injected into a mouse body and is continuously released, so that the processes of mitochondrial injury and pyroptosis are inhibited, and the myocardial fibrosis and cardiac remodeling after myocardial infarction are reduced.

The invention belongs to the technical field of biological medicines, and particularly provides a small molecule compound E229-0305 for preparing a medicine for treating myocardial fibrosis. The small molecule compound E229-0305 can target PTGS2 protein, inhibit fibrosis of myocardial fibroblasts induced by TGF-beta1, reduce proliferation and migration capabilities of the myocardial fibroblasts, inhibit the fibroblasts from being converted into myofibroblasts, and inhibit expression of fibrosis-related genes and proteins. Besides, in a model of myocardial fibrosis after myocardial infarction of a mouse, the small molecule compound E229-0305 improves the cardiac function of the mouse with myocardial infarction and reduces the fibrosis area and collagen deposition of the heart. The small molecule compound E229-0305 can be used as a brand-new targeted PTGS2 small molecule inhibitor for preparing medicines for preventing and treating myocardial fibrosis.

To provide a method of treating cardiac fibrosis in a patient.SOLUTION: The present invention relates to a method of treating cardiac fibrosis in a patient, comprising administering to the patient a therapeutically effective amount of an αV-integrin inhibitor. Pharmacological blockade of αV-containing integrins improved cardiac function and survival after MI by reducing infarct size and attenuating expansion of reactive cardiac fibrosis. Notably, after pharmacological blockade of αV-containing integrins, a total myocardial fibrogenesis area as well as interstitial fibrosis in the remote myocardial area are significantly reduced. These data identify a novel mechanism regulating cardiac fibrosis in response to an ischemic injury and suggest that pharmacological targeting of αV-integrins may provide clinical benefit in the treatment of cardiac fibrosis.SELECTED DRAWING: None

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 belongs to the technical field of medicinal chemistry, and particularly relates to 2, 3-dihydrobenzofuran derivatives and application thereof in preparation of drugs for treating cardiovascular and cerebrovascular diseases. The 2, 3-dihydrobenzofuran derivative disclosed by the invention has a protective effect on H9c2 rat myocardial cell injury caused by H2O2, and can improve the cell survival rate and reduce the LDH release rate; meanwhile, the area of myocardial infarction of mice after myocardial infarction can be remarkably reduced, and the compound has an obvious myocardial protection effect, can be developed into drugs for resisting cardiovascular and cerebrovascular diseases and has a good application prospect. When the 2, 3-dihydrobenzofuran derivative and the luteolin are combined for use, a synergistic effect on treatment of cardiovascular and cerebrovascular diseases is achieved, the synergistic effect of the 2, 3-dihydrobenzofuran derivative and the luteolin can improve the protection effect on the heart, and after the 2, 3-dihydrobenzofuran derivative and the luteolin are combined for use, compared with a single drug, the damage of H2O2 to cells is obviously reduced, and the treatment effect on cardiovascular and cerebrovascular diseases is improved. The cell survival rate is obviously increased, and the LDH release rate is obviously reduced.

The present invention provides the use of a PTMA protein coding sequence in the preparation of a drug for treating myocardial infarction. The PTMA protein coding sequence is a mouse PTMA protein coding sequence, a rat PTMA protein coding sequence, or a human PTMA protein coding sequence. The mouse sequence is shown in Seq ID No. 1, the rat sequence is shown in Seq ID No. 2, and the human sequence is shown in Seq ID No. 3. The PTMA protein coding sequence provided by the present invention can promote the proliferation of damaged myocardial cells, regenerate and repair myocardial tissue, reconstruct the heart morphology after myocardial infarction, restore the heart's pumping function, alleviate the development of cardiac pathological remodeling, prevent the occurrence of heart failure, and has a long-term therapeutic effect on cardiac function after myocardial infarction.

The invention discloses application of hyaluronic acid in post-myocardial infarction heart failure diagnosis and cardiac function prognosis evaluation, belongs to the field of biomarkers, and aims to solve the problems of post-myocardial infarction heart failure diagnosis and cardiac function prognosis evaluation. The technical key point is application of hyaluronic acid HA as a marker in preparation of a product for diagnosis of heart failure after myocardial infarction and prognosis evaluation of cardiac function of a myocardial infarction patient, and the effect is that hyaluronic acid HA can be applied to diagnosis of heart failure after myocardial infarction and prognosis evaluation of cardiac function as a biomarker.

Small molecule stimulators of steroid receptor coactivator-3 (SRC-3) and methods of their use as cardioprotective agents are provided. The small molecule stimulators are useful for promoting cardiac protection and repair and vascular regeneration after myocardial infarction. The compounds are also useful in preventing cardiac hypertrophy and collagen deposition and improving cardiac post-infarction function.

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.

The invention relates to application of arginine diester in preparation of a medicine for preventing and treating cardiovascular diseases, and belongs to the technical field of biological medicines. The invention provides an application of arginine diester in preparation of a medicine for preventing and treating cardiovascular diseases, the structural formula of the arginine diester is as shown in formula I, and y is 2, 3, 4 or 6. According to the arginine diester, the bioavailability of arginine in local cells of the heart is remarkably improved, the biological effect is more effectively played, and the arginine diester has higher heart targeting property and more effectively acts on heart tissues. The composition can significantly improve cardiac function indexes such as ejection fraction, short axis shortening rate and the like of the heart after myocardial infarction and ventricular remodeling, enhance the systolic function of the heart, improve cardiac hypertrophy, reduce the fibrosis area of the heart after myocardial infarction and increase the proportion of cardiac repair type macrophages after myocardial infarction, and is high in biological safety. The long-term treatment cost of cardiovascular diseases is reduced, the medical cost is reduced, and the overall health state and life quality of patients are improved.

The application discloses application of a composition containing tanshinone extract and muscone, and belongs to the technical field of medicines. The compatibility and ratio control of the tanshinone extract and the muscone can inhibit expression and / or secretion of FSTL1 of cardiac fibroblasts at a molecular level, regulate related fibrosis signal pathways, thereby inhibiting a myocardial fibrosis process, and producing a synergistic effect with anti-myocardial injury, improving ventricular structure and function abnormalities after myocardial infarction, and being used for treating cardiovascular diseases such as myocardial infarction, myocardial fibrosis and heart failure after myocardial infarction. The composition of the application comprises the tanshinone extract and the muscone, and can be used for preparing a medicine for preventing and treating cardiovascular diseases with better effects.

The present invention discloses an immunogenic peptide segment for human β1-adrenergic receptor and its application, wherein the amino acid sequence of the immunogenic peptide segment is DEARRCYND, as shown in SEQ ID NO.1. The immunogenic vector vaccine for human β1-adrenergic receptor is prepared by coupling the above-mentioned immunogenic peptide segment of human β1-adrenergic receptor with a carrier, and the carrier is Qβ-2aa bacteriophage virus-like particle protein. The present invention successfully couples the preferentially designed immunogenic peptide segment of human β1-adrenergic receptor with the Qβ-2aa bacteriophage virus-like particle protein carrier to prepare a vector vaccine. The immunogenic vector vaccine can be used to prepare drugs for treating hypertension and improving cardiac remodeling after myocardial infarction.

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.

Activated cardiac fibroblasts are essential for the production of extracellular matrix proteins that accumulate during cardiac fibrosis, and PW1+ cardiac adult stem cells were recently proposed as a cellular source of fibroblasts in the ischemic hearts. Here the inventors identify αV-integrin (or CD51) as an essential regulator of PW1+ cardiac adult stem cells fibrogenic behavior. Inhibition of αV-integrin reduce the profibrotic gene expression profile and the ability to differentiate into fibroblasts of cardiac PW1+ cells. The pharmacological blockade of αV-containing integrins improved cardiac function and survival after MI by reducing infarct size and attenuating the extension of reactive cardiac fibrosis. Notably, the total cardiac fibrotic area as well as interstitial fibrosis in the remote myocardial area are significantly reduced after pharmacological blockade of αV-containing integrins. These data identify a new mechanism that regulates cardiac fibrosis in response to an ischemic injury and suggest that pharmacological targeting of αV-integrin may provide clinical benefit in the treatment of cardiac fibrosis.

The present invention belongs to the field of pharmaceutical technology and specifically relates to the use of a Jingfang preparation in the preparation of a medicament for treating cold-coagulated and blood-stasis-type myocardial infarction. The Jingfang preparation comprises eleven Chinese medicinal herbs: Schizonepeta tenuifolia, Saposhnikovia divaricata, Notopterygium incisum, Angelica dahurica, Bupleurum chinense, Peucedanum chinense, Chuanxiong rhizome, Fructus Aurantii Immaturus, Poria cocos, Platycodon grandiflorum, and Licorice root. Animal experiments have shown that the Jingfang preparation significantly reduces whole blood viscosity and plasma viscosity in rats with myocardial infarction induced by epinephrine hydrochloride and ice water stimulation, with an effect comparable to that of Yangxinshi tablets. The preparation can also alleviate the deterioration of cardiac function and reduce the degree of myocardial damage in rats after myocardial infarction induced by cold stimulation, and has broad application prospects.

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 relates to a conductive hydrogel patch and a preparation method and application thereof, the conductive hydrogel patch comprises an inner layer and an outer layer, the outer layer comprises modified gellan gum, and the inner layer comprises a cross-linked network, nanoparticles and a polymer; the cross-linked network is mainly composed of acrylic acid, methacrylic acid N-succinimide ester, alpha-ketoglutaric acid and chitosan, the nanoparticles comprise polypyrrole nanoparticles coated with dopamine, and the polymer comprises a dendritic polymer which is loaded with a fat-soluble drug and is modified by lauryl sodium sulfate. The preparation method comprises the following steps: preparing modified gellan gum; preparing a dendritic polymer loaded with a fat-soluble drug and modified by lauryl sodium sulfate; preparing the polypyrrole nano particles coated with the dopamine; preparing a cross-linked network; and preparing the conductive hydrogel patch. The conductive hydrogel patch is clear in structural layering, synergistic and efficient in function and capable of achieving multi-dimensional accurate intervention and functional repair of a focus area after myocardial infarction.

The present invention belongs to the field of compositions of biomedical materials and high molecular compounds, and provides a hydrogel capable of regulating the redox homeostasis of the microenvironment, its preparation method and application. The polymer network of the hydrogel capable of regulating the redox homeostasis of the microenvironment is formed by the hybridization cross-linking reaction of catechol-modified hyaluronic acid, carboxylated chitosan, oxidized dextran and iron ions; under physiological conditions, the catechol groups in the hydrogel will undergo autoxidation reaction to generate H<subgt;2< / subgt;O<subgt;2< / subgt>, and at the same time, the iron ions coordinated on the catechol groups in the hydrogel will catalyze the decomposition of H<subgt;2< / subgt;O<subgt;2< / subgt> into water and oxygen, thereby regulating the level of reactive oxygen species in the microenvironment. The hydrogel of the present invention can achieve bidirectional regulation of reactive oxygen species in the pathological microenvironment after myocardial infarction, thereby maintaining the redox homeostasis of the pathological microenvironment after myocardial infarction and improving the regenerative repair ability of the existing hydrogel materials with antioxidant ability to the myocardial tissue after myocardial infarction.

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.