33 results about "Cardiac hypertrophy" patented technology

The health-preserving conditioning tea is prepared from the following raw materials in parts by weight: 3 to 8g of earthworms, 2 to 9g of flos carthami, 4 to 7g of ground beetles, 5 to 10g of leeches, 1.5 to 6g of radix aucklandiae, 3 to 8g of herba verbenae, 2 to 5g of gadflies, 3 to 7g of arisaema cum bile, 6 to 10g of radix salviae miltiorrhizae, 4 to 8g of radix paeoniae rubra, 2 to 6g of bombyx batryticatus, 1.5 to 5g of scorpions and 4 to 9g of folium ginkgo. The conditioning tea has the beneficial effects that the conditioning tea not only can replace traditional western medicines and avoid drug resistance and side effects, but also is convenient to carry and take after being bagged, can relieve and reduce the symptoms of cardiovascular and cerebrovascular plaques, namely blockage, during long-term taking according to the treatment course, can prevent cardiovascular and cerebrovascular diseases, activate blood and promote menstruation, and can be used for treating cardiovascular and cerebrovascular diseases. The traditional Chinese medicine composition has the effects of tonifying qi, preserving health, reducing blood fat and blood pressure, and also can be used for treating diseases such as chest distress, chest pain, cardiac hypertrophy, mitral valve and tricuspid valve regurgitation, myocardial ischemia and the like.

The present application relates to a PROTAC construction based on E3 ubiquitin ligase ZER1 and target protein DVL2 and its application in heart failure treatment. In particular, the present application provides a proteolysis targeting chimera (PROTAC) complex comprising an E3 ubiquitin ligase binding ligand moiety and a target protein binding ligand moiety connected by a linker, wherein the E3 ubiquitin ligase binding ligand is a ZER1 binding ligand, and the target protein binding ligand is a DVL2 binding ligand. The PROTAC molecule in the present application targets DVL2 ubiquitination degradation by recruiting E3 ubiquitin ligase ZER1 to regulate the CaMKII / HDAC4 / MEF2C signaling axis, thereby reducing pathological cardiac hypertrophy and intervening the progression of heart failure, and providing a new therapeutic target for treating cardiac hypertrophy and heart failure caused by pressure overload.

The invention belongs to the technical field of biological medicine and molecular biology, and provides a hypertrophic cardiomyopathy virulence gene MYH7c.794Cgt; the invention relates to T (p.Thr265Ile) and an application thereof. The MYH7 gene mutation is located on the ninth exon, the 794th base is mutated from C to T, namely ACC is mutated to ATC, and the 265th amino acid in the coded amino acid sequence is mutated from threonine to isoleucine. The mutation induces cardiac hypertrophy by disrupting energy metabolism-this defect occurs prior to the occurrence of systolic dysfunction. Along with increasingly prominent status of precision medicine in cardiovascular treatment, a treatment strategy aiming at an upstream pathological process (such as energy homeostasis and mitochondrial dysfunction) provides a way with a wide prospect for preventing and treating MYH7-related hypertrophic cardiomyopathy. MYH7 gene screening has important values in the aspects of promoting early diagnosis, guiding timely treatment intervention and realizing risk-based prevention and management.

The invention discloses a PARP1 inhibitor with methyl-1 'H-spiro [piperidine-4, 2'-quinazoline]-4 '(3' H)-ketone as a mother nucleus and a preparation method and application of the PARP1 inhibitor, a main compound has good PARP1 inhibitory activity (IC50 is at a submicromole level), and compared with a PARP1 inhibitor olaparib on the market, the compound has better anti-myocardial hypertrophy activity, and can be used for preparing a medicine for treating myocardial hypertrophy. The potential of PARP1 as a target spot for treating cardiac hypertrophy is proved, and a potential therapeutic drug is provided for treating cardiac hypertrophy.

The invention belongs to the technical field of biological medicines, and particularly discloses application of colchicine in preparation of a medicine for treating hypertrophic cardiomyopathy. Researches show that after colchicine is used for treatment, pathological changes such as cardiac fibrosis of hypertrophic cardiomyopathy are relieved. Further experimental results show that after colchicine treatment, the proportion of pro-inflammatory macrophages in the cardiac hypertrophy tissue is reduced, the IL-6 level is reduced, and it is prompted that the anti-inflammatory ability of colchicine can improve the microenvironment of the cardiac hypertrophy tissue, so that fibrosis is relieved, and the cardiac function is improved. The invention proves the clinical transformation potential of colchicine in the treatment of cardiac hypertrophy patients. If the medicine is applied clinically in the future, the risk of sudden cardiac death is expected to be reduced by relieving cardiac fibrosis, and a new treatment choice is provided for improving the prognosis of a hypertrophic cardiomyopathy patient.

The present invention provides small molecule PAK1 (P21 Activated Kinase 1) and / or PAK2 (P21 Activated Kinase 2) activators and their use in the prevention and / or treatment of diseases or conditions responsive to PAK1 and / or PAK2 activity or diseases or conditions associated with PAK1 and / or PAK2 inactivity, e.g. cardiovascular diseases or conditions, including cardiac fibrosis, cardiac hypertrophy, cardiac arrhythmias, heart failure and ischaemia / reperfusion injury.

The invention provides application of sedum spectabile total flavonoids in preparation of a medicine for treating pathological cardiac hypertrophy. The sedum spectabile total flavone can inhibit abnormal hypertrophy of cardiac muscle cells, improve arrangement disorder and fibrosis of the cardiac muscle cells, relieve thickening of ventricular walls, improve the diastolic function, delay or reverse pathological cardiac hypertrophy and relieve mitochondrial dysfunction in cardiac muscle tissue with cardiac hypertrophy.

The invention discloses application of a membrane-bound O-acyltransferase structural domain 7 (Mboat7) in preparation of a medicine for treating myocardial hypertrophy, and belongs to the technical field of biology. Research results show that in a mouse cardiac hypertrophy model, compared with a control group mouse, heart weight / body weight, lung weight / body weight, cardiac muscle cell cross sectional area and fibrosis of a cardiac muscle cell specific Mboat7 gene overexpressed mouse are all remarkably reduced, and the cardiac systolic function is remarkably improved; the overexpressed Mboat7 gene can relieve isolated cell myocardial hypertrophy induced by angiotensin II. Particularly, overexpression of the Mboat7 gene can improve damage of mitochondria in myocardial tissue of a cardiac hypertrophy mouse. The results show that the Mboat7 gene overexpression relieves the disease progress of the pathological cardiac hypertrophy, and the Mboat7 or the expression promoter thereof can be used for preparing the medicine for preventing, relieving and / or treating the pathological cardiac hypertrophy.

The invention provides application of dragon's blood and active ingredients thereof in preparation of a medicine for treating heart failure, and belongs to the technical field of biological medicine. It is found for the first time that the dragon's blood can significantly improve the heart function of a heart failure model animal, reduce the level of a heart failure marker and relieve cardiac hypertrophy, cardiac pulmonary edema, myocarditis infiltration and fibrosis; core active components such as genistein and 3-hydroxycinnamic acid are screened and verified, wherein the genistein can reproduce the overall treatment effect of the dragon's blood. The invention also discloses that the core action mechanism of the composition is to promote macrophage VEGFC secretion, increase heart lymphatic vessel density and promote lymphatic vessel neogenesis, and a brand new natural drug candidate scheme and an intervention strategy are provided for heart failure treatment.

The invention belongs to the technical field of gene therapy, and particularly relates to application of an inhibitor of a targeted Pannexin1 gene in preparation of a medicine for preventing or treating myocardial fibrosis. In order to clarify the effect of pan-connexin1 in the cardiac hypertrophy process caused by overload of pressure, the invention provides application of an inhibitor of a targeted Pannexin1 gene in preparation of a medicine for preventing or treating myocardial fibrosis. According to the invention, it is found for the first time that Pannexin1 is an effective target spot for treating myocardial hypertrophy caused by pressure overload, and an expression inhibitor for inhibiting Pannexin1 by targeting the target spot can be used for preparing drugs for treating myocardial hypertrophy caused by pressure overload. Therefore, the invention provides the application of the inhibitor targeting the Pannexin1 gene in preparation of the medicine for preventing or treating the myocardial fibrosis, and a new treatment mode is provided for treatment of the myocardial fibrosis.

The invention belongs to the technical field of biomedicine and biology, particularly relates to a medicine capable of treating diseases related to protein sedimentation, and particularly discloses a medicine for treating or improving diseases or symptoms related to protein sedimentation, the medicine contains Emc3 protein, and the amino acid sequence of the Emc3 protein is shown as SEQ ID No: 1; the nucleotide sequence of the Emc3 protein is as shown in SEQ ID No: 2. The Emc3 can be used as a target gene for screening and preparing drugs for improving cardiac protein sedimentation, cardiac myocardial cell hypertrophy, cardiac hypertrophy, cardiac failure and the like, reducing death caused by protein deposition and prolonging survival time.

The invention belongs to the technical field of biological medicines, and discloses a cardiac function enhancer and application thereof. The active ingredient of the cardiac function enhancer is polyunsaturated phosphatidyl ethanolamine or 3-denitrified adenosine. The polyunsaturated phosphatidyl ethanolamine can be directly used as a key lipid for enhancing the cardiac function. And 2, 3-denitrified adenosine competitively inhibits phosphatidyl ethanolamine methyltransferase to reduce the conversion of phosphatidyl ethanolamine to phosphatidylcholine, so that the level of endogenous polyunsaturated phosphatidyl ethanolamine is improved, and the same effect is indirectly achieved. The invention provides application of the active ingredients in preparation of medicines or nutritional supplements for treating heart diseases, preventing and inhibiting cardiac hypertrophy and improving heart functions.

The invention belongs to the technical field of traditional Chinese medicines, and particularly relates to a modified Zhenwu decoction traditional Chinese medicine compound and application thereof. The traditional Chinese medicine compound of the modified true Wu decoction is prepared from the following raw materials in parts by weight: 10 to 30 parts of radix aconiti lateralis praeparata slices, 6 to 18 parts of sun-dried ginseng, 10 to 30 parts of poria cocos, 8 to 24 parts of raw rhizoma atractylodis macrocephalae, 10 to 30 parts of radix paeoniae alba, 20 to 60 parts of pubescent holly root and 4 to 12 parts of rhodiola rosea. Clinical observation finds that the flavored Zhenwu decoction is an effective drug for resisting HFpEF, and can reverse cardiac hypertrophy of HFpEF mice, relieve pulmonary edema conditions, remarkably improve the diastolic function, improve HFpEF cardiac hypertrophy, improve cardiac diastolic dysfunction, improve myocardial injury and collagen deposition and improve myocardial cell mitochondrial injury.

The invention discloses an application of Gitogenin (Gitogenin, GIT) in preparation of a medicine for preventing or treating hypertrophic cardiomyopathy and diseases caused by the hypertrophic cardiomyopathy. According to the application disclosed by the invention, the prevention or treatment of the hypertrophic cardiomyopathy by the Gitogenin is proposed for the first time, and experiments find that the in-vitro treatment of the Gitogenin can obviously inhibit the phenotype of myocardial cell hypertrophy; gitogenin is applied to gavage treatment on a mouse with hereditary hypertrophic cardiomyopathy caused by gene mutation, and the Gitogenin is found to obviously relieve pathological cardiac hypertrophy of the mouse and improve the cardiac function. The Gitogenin can be used for preparing the medicine for resisting the hereditary hypertrophic cardiomyopathy, and a new way and means are provided for treating the hypertrophic cardiomyopathy; in addition, the Gitogenin is clearly reported to be a main natural steroid component separated from a whole plant of a plant Tribulus longipetaus (a caltrop plant), the biological safety of the Gitogenin to organisms is high, and the Gitogenin has a good application prospect in clinic.

The invention discloses an application of circular RNA circRftn1 in treatment of cardiac hypertrophy, the circRftn1 is the circular RNA found for the first time, circBase ID of the circRftn1 is nucirc0004641, the research finds that the circRftn1 is highly expressed in cardiac muscle tissues of a cardiac hypertrophy cell model and an animal model, the circRftn1 is highly expressed in peripheral blood and cardiac muscle tissues of a cardiac hypertrophy patient, and the circRftn1 is highly expressed in the cardiac muscle tissues of the cardiac hypertrophy cell model and the animal model. The siRNA for inhibiting circRftn1 expression can reduce the myocardial cell volume of a myocardial hypertrophy cell model and an animal model; it is found that the circRftn1 / mumiR-1192 network plays an important role in activating an NF-B p65 signal channel by regulating and controlling TRIM25 / TRIM41 molecular expression, and it is likely that the circRftn1 is inhibited to improve the action mechanism of cardiac hypertrophy.

The invention belongs to the technical field of gene therapy, and particularly relates to application of an inhibitor of a targeted Xirp2 gene in preparation of a medicine for preventing or treating myocardial fibrosis. In order to determine the effect of the actin binding protein Xirp2 in the cardiac hypertrophy process caused by pathological matrix hardness-induced myocardial cell hypertrophy and pressure overload, the invention provides application of an inhibitor of a targeted Xirp2 gene in preparation of a medicine for preventing or treating myocardial fibrosis. The inhibitor is siRNA of which the nucleotide sequence is shown as SEQ ID NO: 1-3 or shRNA of which the nucleotide sequence is shown as SEQ ID NO: 4. The invention finds that Xirp2 is related to myocardial hypertrophy caused by myocardial cell hypertrophy induced by pathological matrix hardness and myocardial hypertrophy caused by pressure overload for the first time, and after expression of Xirp2 is knocked down in vivo and in vitro, myocardial hypertrophy can be relieved. Therefore, the invention develops a new application of the inhibitor targeting the Xirp2 gene, develops a new medicine and a new treatment mode for myocardial fibrosis, and has great significance.

The present application relates to a kind of compound for treating myocardial hypertrophy disease, it is related to the field of biological medicine.The compound can effectively improve the left ventricular systolic function of myocardial hypertrophy mouse, reduce heart weight / body weight, lung weight / body weight, myocardial cell cross-sectional area and fibrosis;Meanwhile, the compound can relieve angiotensin II induced myocardial hypertrophy in vitro.Especially, the compound can improve the damage and dysfunction of mitochondria in myocardial tissue of myocardial hypertrophy mouse, while improving the oxidative phosphorylation level of myocardial cell after angiotensin II stimulation, has the potential of preparation treatment myocardial mitochondrial damage, inhibits myocardial cell hypertrophy, treatment myocardial hypertrophy and heart failure drug.

The invention discloses application of a transcription factor regulatory factor X1 (RFX1) inhibitor in preparation of a medicine for treating cardiac hypertrophy, and belongs to the field of gene application. A myocardial cell specific Rfx1 gene knockout mouse and a same-nest wild type Rfx1fl / fl mouse are taken as experimental subjects, a myocardial hypertrophy animal model is induced through aortic arch constriction, and the result shows that in the mouse myocardial hypertrophy model, the expression of RFX1 is remarkably up-regulated compared with that of a normal group; compared with a same-nest wild type Rfx1fl / fl model mouse, the heart weight / body weight, myocardial cell cross section area and fibrosis of the myocardial cell specific Rfx1 gene knockout mouse are all obviously reduced, the cardiac systolic function is obviously improved, and the results show that the Rfx1 gene knockout relieves the disease progress of pathological myocardial hypertrophy. Aiming at the effects of the RFX1, the inhibitor of the RFX1 can be used for preparing medicines for preventing, relieving and / or treating cardiac hypertrophy and heart failure.

The invention belongs to the technical field of biological medicines, and particularly relates to a medicine for treating hypertrophic cardiomyopathy. The invention finds that S-adenosylmethionine has a remarkable treatment effect on hypertrophic cardiomyopathy. After the intervention of the S-adenosylmethionine, the cardiac hypertrophy degree of a mouse with hypertrophic cardiomyopathy is reduced, and the heart form is obviously improved. Besides, after the intervention of the S-adenosylmethionine, the expression quantity of myocardial injury symbolic genes Nppa and Nppb of a mouse with hypertrophic cardiomyopathy is reduced, the cardiac fibrosis is reduced, and the sectional area of myocardial cells is reduced. The treatment effect of the S-adenosylmethionine on the hypertrophic cardiomyopathy is not inferior to that of a targeted drug mavacamten, and the S-adenosylmethionine does not inhibit the systolic function of the heart, so that the S-adenosylmethionine has higher safety and provides more treatment strategies for the treatment of the hypertrophic cardiomyopathy.

The invention belongs to the field of heart disease treatment, and provides application of a cortex fraxini extract in preparation of a medicine for resisting heart failure. The application proves that oral administration and intraperitoneal injection of the cortex fraxini extract can obviously improve the heart function of a mouse with heart failure and relieve cardiac hypertrophy and fibrosis, and the mechanism of the cortex fraxini extract is possibly related to inhibition of inflammatory response and regulation of fibrosis-related factor expression.

A pharmaceutical composition containing an effective amount of cannabidiol (CBD) for use in the treatment or prevention of cardiac conditions, as well as related methods and uses. [Solution] Cardiac conditions include heart failure, acute myocarditis, toxicity caused by anticancer therapy, acute pericarditis, cardiac sarcoidosis, inflammatory cardiomyopathy, and atherosclerosis, as well as related uses and methods. This disclosure shows that CBD is effective in (i) reducing cardiac hypertrophy; (ii) reducing cardiac fibrosis; (iii) reducing BNP levels; (iv) reducing cytokine IL1β levels; (v) reducing cytokine IL6 levels; (vi) reducing CD69 levels; (vii) increasing cytokine IL10 levels; and (viii) combinations thereof. The compositions are preferably adapted for parenteral administration.

The application belongs to the field of medicine, and specifically discloses application of a small molecule compound KA-C1 in preparation of a medicine for preventing or treating cardiac hypertrophy, cardiac fibrosis and / or heart failure. The application finds that kynurenine-3-monooxygenase (KMO) is an effective medicine target for treating pathological cardiac hypertrophy and cardiac fibrosis through research. Through computer-aided virtual screening, the application finds a KMO-specific agonist KA-C1, and KA-C1, as a medicine active ingredient, can directly stimulate KMO protein activity, thereby effectively resisting pathological cardiac hypertrophy and cardiac fibrosis, and further preventing or treating heart failure. Therefore, the discovery of the small molecule compound KA-C1 provides a new medicine target strategy for treating pathological cardiac hypertrophy, cardiac fibrosis and heart failure, and has important and wide application prospects.

The invention discloses an application of an MCP-1 inhibitor in preparation of a medicine for preventing and treating aging-related pathological myocardial hypertrophy, the experiment reveals that MCP-1 is an aging-related pathological myocardial hypertrophy core regulatory factor for the first time, and the MCP-1 is used for up-regulating the protein expression of GATA4, IL-17A, NF-kB-p65 signals, alpha-SMA and Collagen I by activating an IL-17A / MCP-1 / CCR2 / IL-17A signal loop, so that the effect of preventing and treating the aging-related pathological myocardial hypertrophy is achieved. Further, myocardial cell senescence and senescence-related secretory phenotypes, hypertrophy and fibrosis are induced. Experiments prove that the MCP-1 inhibitor can be used for preventing and treating the SA-PCH, can improve the SA-PCH induced by Ang II and / or IL-17A, is free of liver and kidney toxicity and can obviously improve liver and kidney function decline induced by Ang II, and a new way is provided for clinical treatment of the SA-PCH.

The application discloses application of 1,2,3,4,6-O-galloyl glucose in preparation of a drug for preventing and / or treating myocardial hypertrophy, and belongs to the technical field of biological medicine. The application proves for the first time that PGG can significantly improve cardiac dysfunction induced by TAC operation, inhibit increase of heart volume and weight, myocardial cell hypertrophy, down-regulate expression of myocardial hypertrophy markers Nppa, Nppb and Myh7, and block excessive activation of an AKT / ERK signal path. Therefore, PGG can effectively prevent and / or treat pathological myocardial hypertrophy, and has a clear clinical application prospect.

The invention discloses application of rubimaillin in preparation of a medicine for treating or preventing pathological cardiac hypertrophy, and belongs to the field of biological medicine. The invention provides an application of MLG (rubimaillin) in preparation of a medicine for treating or preventing pathological cardiac hypertrophy and a pharmaceutical composition of the MLG. The pathological cardiac hypertrophy comprises types caused by pressure load, hereditary or inflammatory factors. The active ingredient of the pharmaceutical composition is rubimaillin. Through in-vitro and in-vivo researches, the application value of the MLG in the medicine for preventing or treating pathological cardiac hypertrophy is disclosed for the first time, and a new way and means are provided for treatment of related diseases.

The invention discloses an application of ganoderic acid A in preparation of an anti-heart failure drug. Researches find that the ganoderic acid A (formula I) has an effect of inhibiting mouse cardiac hypertrophy induced by aortic constriction (TAC), and the ganoderic acid A can relieve the mouse cardiac hypertrophy induced by the TAC. The ganoderic acid A can inhibit cardiac fibrosis of a model mouse and improve the diastolic function of the mouse. Therefore, the ganoderic acid A can be applied to preparation of the anti-myocardial hypertrophy medicine. The invention provides a new effective technical means for treating cardiac hypertrophy, and has a wide application prospect. Formula I

A method for reducing pathological cardiac hypertrophy and / or inducing physiological cardiac hypertrophy by administering Nigella sativa or an extract thereof to a subject in need thereof, especially to an athletic subject in order to reduce exercise-induced pathological cardiac hypertrophy. A composition comprising Nigella sativa for use in said method.

The invention relates to the field of medicine application, in particular to application of monochorioside in preparation of heart failure resisting medicine. According to the invention, experiments firstly verify that the crystal orchid glycoside can obviously improve cardiac diastolic dysfunction, myocardial hypertrophy and myocardial fibrosis and reduce the oxidative stress level of myocardial cells; the traditional Chinese medicine composition is beneficial to improving the diastolic activity of the left ventricle of the senescent heart, can obviously reduce the cardiac hypertrophy index and the cardiac muscle cell area of the senescent heart, and has a certain degree of improvement on heart injury caused by heart senescence, and the higher the concentration is, the more remarkable the improvement effect is. According to the invention, the anti-heart-failure medicine is prepared by taking monochorioside as an active ingredient and a pharmaceutically acceptable carrier or auxiliary material.

The invention relates to application of an SOAT1 inhibitor in preparation of drugs for preventing and treating myocardial hypertrophy related diseases, and belongs to the technical field of biological medicines. The invention provides application of an SOAT1 inhibitor in preparation of drugs for preventing and treating myocardial hypertrophy related diseases. The relationship between the SOAT1 gene and cardiac hypertrophy is found, the mechanism of the SOAT1 gene and cardiac hypertrophy is further elaborated, and by inhibiting the activity of the SOAT1 gene or the protein of the SOAT1 gene, the heart size is recovered, the cross sectional area of cardiac muscle cells is remarkably inhibited, myocardial fibrosis is improved, and the disease progress of pathological cardiac hypertrophy is restrained. The invention also provides an SOAT1 inhibitor, which comprises a small molecule compound F0808-1832, so as to inhibit SOAT1 gene expression and protein activity, lay a solid theoretical basis for preventing and treating myocardial hypertrophy related diseases, and provide a medicine with a good treatment effect.

A method of treating a subject with a disease where the disease is selected from the group consisting of hypertension, cardiac hypertrophy, cardiomyocyte enlargement, myocardial fibrosis, liver fibrosis, and cardiac fibrosis is provided. The method involves administering to the subject an effective amount of a fibroblast growth factor (FGF) 21 inhibitor.