202 results about "Myocardial hypertrophy" patented technology

The invention provides a pyrazolopyrimidine compound shown as a structural formula (I), a pharmaceutical composition taking the pyrazolopyrimidine compound as an active component, a preparation method of the pyrazolopyrimidine compound and the pharmaceutical composition as well as an application of the pyrazolopyrimidine compound and the pharmaceutical composition in preparation of a TRPC6 (Transient Receptor Potential Channel 6) adjustor probe medicine and related medicines for preventing and treating glomerulopathy and myocardial hypertrophy. The pyrazolopyrimidine compound and derivatives provided by the invention can be used to prepare medical preparations in various forms which comprise oral liquids, injections, pulmonary inhalation preparations and transdermal preparations, specifically injections, oral liquids, troches, capsules, granules, aerosols, dry powder inhalation, patches and the like.

The invention provides the construction for a farnesyl pyrophosphoric acid synthetase RNA (Ribonucleic Acid) interference recombinant lentivirus vector, which comprises the following steps of: sieving the most effective target sequence of an FDS (farnesyl diphosphate synthase) gene RNAi (RNA interference) in a tool cell 293T cell, synthesizing the double-stranded DNA of the most effective target sequence, connecting to a pGCSIL-GFP vector and successfully constructing the recombinant vector through enzyme cutting, sequencing and identification. Researches indicate that the constructed RNA interference vector LV-sh-FDS can downwards modulate the expression of an FDS mRNA (Messenger RNA) level in a neonatal rat cardiac myocyte, simultaneously can downwards modulate the expression of myocardial hypertrophy markers such as cell areas and marker genes beta-MHC (Myosin Heavy Chain) and BNP (Brain Natriuretic Peptide), additionally can effectively inhabit the activity of RhoA while downwards modulating the FDS, can be applied in preparing medicaments for treating myocardial hypertrophy diseases and also can be applied in preparing medicaments for cholesterol metabolic control.

A cardiac electro-stimulatory device and method for operating same in which stimulation pulses are distributed among a plurality of electrodes fixed at different sites of the myocardium in order to reduce myocardial hypertrophy brought about by repeated pacing at a single site and / or increase myocardial contractility. In order to spatially and temporally distribute the stimulation, the pulses are delivered through a switchable pulse output configuration during a single cardiac cycle, with each configuration comprising one or more electrodes fixed to different sites in the myocardium.

The present invention relates to compounds having a naphthyridine scaffold, and stereoisomeric forms, prodrugs, solvates, hydrates and / or pharmaceutically acceptable salts of these compounds as well as pharmaceutical compositions containing at least one of these naphthyridine derivatives together with pharmaceutically acceptable carrier, excipient and / or diluents. Said naphthyridine compounds have been identified as inhibitors of the protein kinase ROCK2, also known as Rho-kinase, and are useful for the treatment of cancers (tumor growth and metastases), erectile dysfunction, cardiovascular diseases, hypertension, angina pectoris, cerebral ischaemia, cerebral vasospasm, myocardial ischaemia, coronary vasospasm, heart failure, myocardial hypertrophy, atherosclerosis, restenosis, spinal cord injuries, neuronal degeneration, thrombotic disorders, asthma, glaucoma, inflammation, anti-viral diseases (e.g. HIV), and osteoporosis.

A cardiac electro-stimulatory device and method for operating same in which stimulation pulses are distributed among a plurality of electrodes fixed at different sites of the myocardium in order to reduce myocardial hypertrophy brought about by repeated pacing at a single site and / or increase myocardial contractility. In order to spatially and temporally distribute the stimulation, the pulses are delivered through a switchable pulse output configuration during a single cardiac cycle, with each configuration comprising one or more electrodes fixed to different sites in the myocardium.

The invention relates to medical examination and diagnosis methods and instruments, in particular to a multi-dimensional electrocardiosignal imaging system and method. The body surface electric potential mapping technology and the electrocardio vector technology are integrated, a new non-invasive platform is provided for recording the heart-across-myocardium electrical activity information, and in other words, a new non-invasive body surface heart-across-myocardium electrical activity information imaging method and technology which are formed by combining the vector center 0 point galvanic coupling and body surface electric potential mapping technology and are similar to satellite positioning are provided. The non-invasive electrocardio function imaging method and technology for detecting heart-across-myocardium electrocardio activity information with the dissection positioning as a basis are provided. According to the multi-dimensional electrocardiosignal imaging system and method, the arrhythmia reason can be determined, the cardiac muscle diseases such as myocardial hypertrophy, cardiomyopathy, myocardial infarction and myocarditis can be diagnosed, and a brand new diagnosis tool is provided for fast diagnosing the heat diseases in real time.

A cardiac electro-stimulatory device and method for operating same in which stimulation pulses are distributed among a plurality of electrodes fixed at different sites of the myocardium in order to reduce myocardial hypertrophy brought about by repeated pacing at a single site and / or increase myocardial contractility. In order to spatially and temporally distribute the stimulation, the pulses are delivered through a switchable pulse output configuration during a single cardiac cycle, with each configuration comprising one or more electrodes fixed to different sites in the myocardium.

The invention belongs to the traditional Chinese pharmaceutics field, and relates to an application of traditional Chinese medicine radix scrophulariae to the preparation of a drug for preventing and curing cardiac hypertrophy, hypertrophic cardiomyopathy and chronic heart failure. The invention researches the effect of the cardiac hypertrophy and ventricle reconstruction model of a plurality of mice and rats on the traditional Chinese medicine radix scrophulariae. The experimental results show that the radix scrophulariae water or the alcohol abstracts has evident function for preventing the cardiac hypertrophy, the ventricular remodeling and the chronic heart failure caused by various reasons, the mechanism is obviously related with the excessive activation of the neuroendocrine system such as a suppressing renin-angiotensin-aldosterone system and is related with the functions of blood pressure reduction, heart beat slowing and hemodynamics improvement. The figwort can be used for preparing the drug for preventing the diseases of cardiac hypertrophy, hypertrophic cardiomyopathy and chronic heart failure and for reducing the possibility of the incidence rate of arrhythmia and the sudden death of patients with cardiac hypertrophy, hypertrophic cardiomyopathy and chronic heart failure.

A low common salt soy sauce, which has good flavor, significantly suppresses elevation of blood pressure, prevents cardiac hypertrophy, and is also available as special nutritious food, is obtained. 1.0% to 10.0% by weight of potassium chloride and 0.1% to 5.0% by weight of γ-aminobutyric acid are added to a reduced common salt soy sauce, so as to obtain a low common salt soy sauce of issue. Otherwise, a KCl-containing low common salt soy sauce is obtained by: (1) a common production method of soy sauce, in which a mixed solution consisting of KCl and common salt is used as mother water; (2) a method of subjecting a soy sauce obtained using saline solution as mother water to electrodialysis, a membrane treatment, or the like, so as to eliminate common salt from the above soy sauce, and then adding KCl thereto; or other methods. Thereafter, γ-aminobutyric acid is added to the above KCl-containing low common salt soy sauce, so as to obtain a low common salt soy sauce comprising 0% to 10% by weight of common salt, 1.0% to 10.0% by weight of potassium chloride, and 0.1% to 5.0% by weight of γ-aminobutyric acid.

The invention relates to a preparation method and an application of an effective part of dracocephalum heterophyllum benth. The method comprises the steps that an aboveground part of the dracocephalum heterophyllum benth is smashed, extracted by an organic solvent, namely alcohol, and subjected to macroporous resin separation and purification to form the effective part of the dracocephalum heterophyllum benth. A preliminary activity screening test proves that the effective part of the dracocephalum heterophyllum benth obtained by the method has functions of lowering renal hypertension and rat blood pressure, and enhancing diastole and systole, and can also effectively prevent and treat hypertension complications including myocardial hypertrophy, renal injuries and vascular endothelial injuries. The method is simple in technology, low in production cost, and easy to control, and does not require high temperature or high pressure equipment, and the quality of the effective component is stable.

The invention provides a construction method for a miRNA (micro Ribonucleic Acid) transgenic mice model. In the construction method, a transgenic mouse with overexpression miR-27b in a myocardial cell is established by using a transgenic technology; the systematic phenotyping on the transgenic mouse finds that the mouse possibly has myocardial hypertrophy and heart function damage; the basic pathological changes of the mouse are similar to those of human hearts, therefore, with the establishment of the transgenic mouse model, a favorable animal model for researching the heart disease nosogenesis and researching and developing new drugs is provided.

The invention disclosure an application of sinomenine in the preparation of a medicament for preventing and treating myocardial hypertrophy or a disease based on the myocardial hypertrophy. According to the invention, myocardium of a little mouse is stimulated and induced by means of a beta-receptor stimulant, isoprenaline, and a myocardial hypertrophy model for the little mouse is duplicated; the myocardial hypertrophy of a big rat is induced by means of abdominal aortic coarctation, and a myocardial hypertrophy model for the big rat is duplicated; Chinese herbal medicine monomer, sinomenine, of different doses is applied to the myocardial hypertrophy model for the little mouse and the myocardial hypertrophy model for the big rat respectively. After experimental studies on entire animals in terms of pharmacodynamics, a positive treatment effect is achieved, and a foundation is provided for the screening of new drugs.

The invention discloses application of adenine nucleotide translocator 1 (ANT1), and relates to the field of the treatment of cardiovascular diseases. Through down-regulating the level of the sulfydryl nitrosylation modification of the ANT1 in a myocardial cell, the occurrence of myocardial hypertrophy is effectively inhibited. A method comprises the following steps of transfecting a myocardial cell by utilizing an adenovirus with the modification site mutation of cysteine, and regulating and controlling the expression of the sulfydryl nitrosylation modification of ANT1 protein in a cell, andalso comprises the following steps of specifically transfecting the heat tissue of a mouse by utilizing an adeno-associated virus with the modification site mutation of the cysteine, and regulating and controlling the expression of the sulfydryl nitrosylation modification of ANT1 protein in the heart tissue. Therefore, the sulfydryl nitrosylation modification of the ANT1 protein can be used as a new important target for clinically treating the myocardial hypertrophy, and has potential clinical application value in the prevention and treatment of the myocardial hypertrophy.

The invention discloses application of a polypeptide able to specifically bind TRB3 or polypeptide derivative or polypeptide chimeric peptide in preparation of drugs or vaccines for prevention and / or treatment of hypertensive myocardial hypertrophy. The polypeptide has an amino acid sequence shown as SEQ ID NO:1, the amino acid sequence of the polypeptide derivative is a SEQ ID NO:1 derived amino acid sequence that is obtained by subjecting the amino acid sequence shown as SEQ ID NO:1 to substitution, deletion or adding by one or several amino acid residues and has the same activity to an amino acid residue sequence of SEQ ID NO:1, and the polypeptide chimeric peptide is formed by connecting the polypeptide or polypeptide derivative with a cell-penetrating peptide. The invention also further discloses a nucleotide fragment encoding the polypeptide or polypeptide derivative, and application of pharmaceutical compositions containing the polypeptide or polypeptide derivative or polypeptide chimeric peptide and the nucleotide sequence thereof in preparation of drugs or vaccines for prevention and / or treatment of hypertensive myocardial hypertrophy.

The invention belongs to the technical field of medicines, and particularly relates to 5'-AACGTT-3'-containing oligonucleotides, a functional analogue of the oligonucleotides, and usage of the oligonucleotides or the functional analogue of the oligonucleotides for preventing and curing myocardial hypertrophy and chronic heart failure. The oligonucleotides and the usage realize the function of the 5'-AACGTT-3'-containing oligonucleotides by using myocardial cells and animal hypertrophy models acknowledged in the academia at home and abroad. The experimental result shows that the 5'-AACGTT-3'-containing oligonucleotides can obviously restrain the expression of a landmark protein ANF (atrial natriuretic factor) and a beta-MHC (major histocompatibility complex) gene of the myocardial hypertrophy, and can restrain the increase of a superficial area of the myocardial cell, and the restrain function of the oligonucleotides depends on the dosage of the oligonucleotides.. In the whole experiment, the 5'-AACGTT-3'-containing oligonucleotides can obviously restrain the myocardial hypertrophy and the increase of the heart-body ratio, and the happening of myocardial necrosis can be reduced. The experiment result disclosed by the invention prompts that the 5'-AACGTT-3'-containing oligonucleotides is the medicine for effectively curing the myocardial hypertrophy and the heart failure.

The invention discloses a (micro ribose nucleic acid)-874 and an application of a miRNA-874 antisense nucleotide, and in particular relates to the application of the miRNA-874 antisense nucleotide in preparing pharmaceutical compositions for treating and preventing serious heart diseases (myocardial hypertrophy and myocardial fibrosis) and the application of the miRNA-874 antisense nucleotide in preparing the pharmaceutical compositions for diagnosing or prognosing the heart diseases. The miRNA-874 antisense nucleotide can control cardiac hypertrophy and cardiomyocyte hypertrophy and also has the functions of improving a cardiac function and inhibiting cardiac structure remodeling and cardiac fibering. The miRNA-874 antisense nucleotide can be used as a novel target of drug action, has a function of controlling the myocardial hypertrophy and has an important meaning for clinically preventing and treating heart diseases of cardiac fibering, coronary heat disease, heart failure and the like which are caused by cardiomyocyte hypertrophy.

The invention relates to a method for preparing CNPase mutant zebra fish, and confirms that a mutant model can spontaneously generate bradycardia and even heart failure accompanied by severe heart failure. According to the invention, a CRISPR-Cas9 technology is combined with a microinjection technology, CNPase is specifically knocked out, a CNPase mutant F1 generation is prepared, and confirmation is performed through a Sange sequencing method; and through hybridizing and screening, a zebra fish homozygous mutant strain with heart specificity marked with green fluorescence is prepared, and it is confirmed that the CNPase homozygous mutant zebra fish can spontaneously generate cardiac hypertrophy and partially develop to heart failure through cardiology and kinetics indexes. The CNPase mutant zebra fish is prepared, an animal model is provided for researching functions of CNPase, and particularly great convenience is provided for researching related diseases of bradycardia accompanied by severe heart failure.

The invention discloses a pharmaceutical composition of targeting circRNA (circular Ribonucleic Acid). The pharmaceutical composition comprises MFACR-siRNA (small interfering Ribonucleic Acid) nucleotide, a pharmaceutically acceptable carrier or virus carrier and an auxiliary material; the carrier is one or more of chitosan, cholesterol, nanoparticles and liposome, preferably, the liposome; the auxiliary material is one or more of mannitol, a phosphate buffering solution and saline, preferably, the phosphate buffering solution; the content of the MFACR-siRNA is 0.8 to 1.5 micrograms; the mass ratio of the MFACR-siRNA to the liposome is 1 to 1.25; the mass ratio of the carrier to the auxiliary material is 1 to 200. The pharmaceutical composition is used for treating and preventing myocardial infarction, myocardial ischemial injury, myocardial hypertrophy and myocardial fibrosis, and is dosed in an oral administration or injection manner; the injection is intravenous injection, muscle injection, intracoronary injection or direct myocardial injection. Compared with the prior art, the selected raw materials are scientific and reasonable; a preparation process is simple and the drug action is obvious; the application range is wide, the utilization is safe and reliable and the application is environment-friendly.

The invention discloses an experimental method of a long non-coding RNA up-regulation gene in myocardial hypertrophy; the method is characterized in that the levels of lncRNATUG1, miR-497 and myocardial cell enhancement factor 2CmRNA are evaluated through qRT-PCR (quantitative reverse transcription-polymerase chain reaction), western blot measurement is carried out to determine the expression of MEF2C protein, and the endogenous interaction among TUG1, miR-497 and MEF2C is proved through a dual-luciferase reporter gene and RNA immunoprecipitation experiment. The overexpression of the MiR-497 mediates the protective effect of TUG1 knock-down in the cardiac hypertrophy induced by AngII. In addition, the TUG1 regulates the expression of MEF2C by spongizing miR-497. The knock-down of the TUG1 at least partially rescues AngII-induced myocardial hypertrophy by targeting the miR497 / MEF2C axis, and highlights a novel and promising therapeutic target for treating the myocardial hypertrophy.

The invention discloses function and application of a Caspase activation and recruitment domain 3 (Card3) gene in a coronary atherosclerotic heart disease. The Card3 gene knockout mice and heart specific Card3 transgenic mice are taken as objects, and a research is carried out on a myocardial infarction model caused by blocking mice heart ramus descendens anterior arteriae coronariae sinistrae. The result proves that compared with WT mice, the cardiac infarction proportion, and the degrees of myocardial hypertrophy and fibrosis of the Card3 gene knockout mice are obviously inhibited, and the cardiac function is obviously improved; the phenotype of the Card3 transgenic mice is contrary to that of the Card3 gene knockout mice. Consequently, the Card3 gene can promote and increase development and progression of the coronary atherosclerotic heart disease, the Card3 can be used as a drug target for screening the drugs for treating the coronary atherosclerotic heart disease, and the inhibitor of the Card3 can be applied to preparation of a drug for treating the coronary atherosclerotic heart disease.

The invention discloses a function and an application of TRIM32 (Tripartite motif 32) in treating myocardial hypertrophy and belongs to the field of gene functions and applications. The mutual relation between expression of TRIM32 and myocardial hypertrophy is determined, a research result proves that in a model where myocardial hypertrophy occurs, the expression of TRIM 32 is remarkably reduced than that of a normal group; if expression of TRIM 32 is inhibited, activation of an AKT signal path is remarkably promoted, myocardial hypertrophy and fibrosis are promoted, and the cardiac function is deteriorated; if overexpression of TRIM 32 is promoted, activation of the AKT signal path is remarkably inhibited, myocardial hypertrophy and fibrosis are inhibited, and the cardiac function is protected. Therefore, TRIM32 can be taken as a target gene and used for screening or preparing a drug for protecting the cardiac function, preventing cardiac fibrosis and / or preventing, relieving and / or treating myocardial hypertrophy, and a new effective way is provided for treatment of myocardial hypertrophy.

The invention belongs to the technical field of biology, and particularly relates to an EZH2 variable splicing site and an application thereof. Specific siRNA is used for knocking down two subtypes ofEZH2-L and EZH2-S respectively, and myocardial hypertrophy and heart failure models are established at the cellular level and the animal level respectively. Results show that after the EZH2-L is knocked down, the expression level of a myocardial hypertrophy pathological gene is obviously reduced, the myocardial cell area is reduced, and the heart weight is reduced; and after the EZH2-S is knockeddown, the expression level of the myocardial hypertrophy pathological gene is remarkably increased, the myocardial cell area is increased, the heart weight is increased, and the situation prompts that the EZH2-L and the EZH2-S have the effects of promoting and inhibiting myocardial hypertrophy and heart failure respectively. In addition, after the EZH2-L is knocked down, tumor cell proliferationis inhibited, and knock-down of the EZH2-S has no influence on tumor cell proliferation. The invention provides a new target and a new strategy for research and development of medicines for treating EZH2 gene related diseases.

The invention discloses function and application of a Caspase activation and recruitment domain 3 (Card3) gene in a coronary atherosclerotic heart disease. The Card3 gene knockout mice and heart specific Card3 transgenic mice are taken as objects, and a research is carried out on a myocardial infarction model caused by blocking mice heart ramus descendens anterior arteriae coronariae sinistrae. The result proves that compared with WT mice, the cardiac infarction proportion, and the degrees of myocardial hypertrophy and fibrosis of the Card3 gene knockout mice are obviously inhibited, and the cardiac function is obviously improved; the phenotype of the Card3 transgenic mice is contrary to that of the Card3 gene knockout mice. Consequently, the Card3 gene can promote and increase development and progression of the coronary atherosclerotic heart disease, the Card3 can be used as a drug target for screening the drugs for treating the coronary atherosclerotic heart disease, and the inhibitor of the Card3 can be applied to preparation of a drug for treating the coronary atherosclerotic heart disease.

The invention provides application of 3-hydroxyphenylacetic acid (3-HPA) in preparation of a drug for improving ventricular pathological reconstruction and / heart failure after myocardial infarction, and belongs to the technical field of biomedicine. The 3-HPA can improve cardiac functions after myocardial infarction, reduce heart fibrosis after myocardial infarction and improve the size of cardiacmuscle cells after myocardial infarction. Mouse animal model experiments show that the 3-HPA can improve cardiac functions of mice after rejection of intestinal florae from myocardial infarction miceby antibiotic treatment, reduce heart fibrosis after rejection of intestinal florae from myocardial infarction mice by antibiotic treatment and inhibit myocardial hypertrophy after rejection of intestinal florae from myocardial infarction mice by antibiotic treatment.

The invention relates to application of a qi-tonifying dripping pill containing radix astragali and root of red-rooted salvia to preparation of a medicament for improving myocardial fibrosis and myocardial hypertrophy. The qi-tonifying dripping pill containing radix astragali and root of red-rooted salvia is refined from active ingredients in radix astragali, root of red-rooted salvia, pseudo-ginseng and dalbergia heartwood extracted by modern technology. The invention aims to provide application of qi-tonifying dripping pill containing radix astragali and root of red-rooted salvia to preparation of the medicament for improving myocardial fibrosis and inhibiting further myocardial hypertrophy. According to the application in the invention, after generation of ventriculus sinister hypertrophy, the qi-tonifying dripping pill containing radix astragali and root of red-rooted salvia can improve myocardial fibrosis, substantially inhibit increase of wall thickness cardiac index and body mass index in ventriculus sinister diastasis, increase ejection fraction and shortening fraction of the ventriculus sinister and reduce scope of myocardial fibrosis.

The invention discloses circRNA MNCR nucleotide, a circRNA MNCR nucleotide containing pharmaceutical composition and application thereof. The pharmaceutical composition comprises the circRNA MNCR nucleotide, auxiliary materials, a virus vector or an embedding carrier, wherein the embedding carrier is cholesterol, nanoparticles or liposome and is preferably liposome; the virus vector is one or more of an adenovirus vector, a lentiviral vector and a retroviral vector and is an adenovirus vector preferably; the auxiliary material is one or more of mannitol, phosphate buffer and normal saline and is phosphate buffer preferably; infection titer of the circRNA MNCR virus vector is 10<16>PFU, and a mass ratio of the circRNA MNCR nucleotide to the liposome is 1:1.25; a mass ratio of the virus vector or the embedding vector to the auxiliary material is 1:200. The circRNA MNCR nucleotide and the circRNA MNCR nucleotide containing pharmaceutical composition can be used for prevention and treatment of myocardial hypertrophy, myocardial fibrosis, coronary heart disease and heart failure and prevention of myocardial fibrosis and myocardial remodeling. A preparation process of the pharmaceutical composition is simple, and evident efficacy, convenience in use and environment friendliness in treatment are realized.

The invention relates to the application of CP-1 siRNA in treating AngII induced cardiac hypertrophy. Experimental study proves that the CP-1 siRNA can inhibit cardiac hypertrophy in mice induced by AngII, weakens the degree of ventricular dilatation and the thickness of a ventricular wall, inhibits the expression of marker protein ANF, beta-MHC of the cardiac hypertrophy, inhibits cardiac fibrosis, and is an effective novel cardiac hypertrophy treatment drug.

The invention discloses application of a Vinexin-beta gene in coronary atherosclerotic heart disease, and belongs to the field of functions and application of the gene. According to the invention, Vinexin-beta knockout mouse and heart specificity Vinexin-beta transgenic mouse serve as experimental subjects and mouse heart ramus descendens anterior arteriae coronariae sinistrae (LAD) is blocked to form a myocardial infarction model, and a result shows that, compared with a WT control mouse, the Vinexin-beta knockout mouse is significantly inhibited in myocardial infarction proportion, myocardial hypertrophy and fibrosis degree and is remarkably better in heart functions, while the heart specificity Vinexin-beta transgenic mouse is obviously more serious in myocardial infarction proportion, myocardial hypertrophy and fibrosis degree and is remarkably worse in the heart functions, showing that the Vinexin-beta gene can promote and enhance occurrence and development of the coronary atherosclerotic heart disease. Therefore, the Vinexin-beta gene can serve as a drug target to screen medicines for treating the coronary atherosclerotic heart disease, and a Vinexin-beta inhibitor can be used for preparing a medicine for treating the coronary atherosclerotic heart disease.

The invention belongs to novel application of plantamajoside in resistance of myocardial hypertrophy and particularly relates to application of plantamajoside in preparation of anti-myocardial hypertrophy drugs. An isoproterenol is adopted for inducing a myocardial hypertrophy model of a mouse and an H9c2 cardiomyocyte hypertrophy model, and meanwhile, intervention is carried out on plantamajosidedifferent in concentration; cardiac functions of the mouse are evaluated through ultrasound, the heart of the mouse and the left ventricular are weighed, and the myocardial hypertrophy degree of themouse is evaluated. The area of H9c2 cardiomyocytes is observed by means of fluorescence staining, and results show that plantamajoside has a protection effect on isoproterenol-induced myocardial hypertrophy of the mouse and an inhibitory effect on isoproterenol-induced H9c2 cardiomyocyte hypertrophy. Plantamajoside is expected to be developed for clinical use in the anti-myocardial hypertrophy drugs.

The invention relates to an artificial zinc finger protein transcription factor which can activate the A20 gene expression, and the application of the artificial zinc finger protein transcription factor. The preparation method comprises the preparation of a zinc finger motif polypeptide bonded with the A20 gene promoter region target sequence specificity, as well as the synthesis of an artificial transcription factor; the artificial transcription factor comprises a binding region, a functional region, a nuclear localization signal and a transmembrane region; the connection order is the transmembrane region-the nuclear localization signal - the binding region - the functional region; the prepared polypeptide containing 3 to 6 zinc finger sequences is syncretized into the functional region of NF-p65 or VP64 and joined with the nuclear localization signal; 9 arginines or 12 amino acids of a Tat protein are added to the N-terminal to serve as a protein transduction region. The invention can effectively span the cell membranes to enter the cells to activate the expression of the A20 gene, and has good anti-vascular restenosis, atherosclerosis sclerosis, cardiac hypertrophy, serious inflammatory injury and other performances; the invention can be applied to the preparation of the cell protection drugs for overcoming the rejection of organ transplants or cardiac hypertrophy or serious inflammatory injury.