11 results about "Ischemic heart" patented technology

Provided is a method for screening myocardial therapeutic targets for ischemic heart failure by using single-cell sequencing, which method comprises the following steps: S1, sample preparation; S2, construction of a single-cell expression matrix; S3, cell quality control; S4, cell type annotation; S5, cell communication analysis; and S6, co-expression network analysis. The provided method for screening myocardial therapeutic targets for ischemic heart failure by using single-cell sequencing comprises performing single-cell sequencing on hearts of healthy mice and IHF mice, screening for cell types with significant differences in cardiac transcriptional profiles of the healthy mice and IHF mice, then exploring interaction characteristics of various types of cells in malignant fibrotic IHF hearts, revealing potential regulatory modules and pathways related to malignant myocardial fibrosis in single-cell expression data of IHF hearts, and performing screening to obtain Pdgfb and Tnfsf12 genes which can be used as therapeutic targets for treating myocardial fibrosis in ischemic heart failure.

The invention relates to a traditional Chinese medicine composition for treating ischemic heart failure and a preparation method thereof, and belongs to the field of traditional Chinese medicine pharmacy, and the traditional Chinese medicine composition is prepared from the following raw material medicines in parts by weight: 5-15 parts of cassia twig, 5-15 parts of bighead atractylodes rhizome, 5-15 parts of poria cocos, 6-12 parts of rhizoma zingiberis, 5-15 parts of acanthopanax, 10-30 parts of fructus polygoni orientalis, 3-9 parts of verbena, 6-12 parts of dogwood and 3-9 parts of honey-fried licorice root. The composition can remarkably reduce the level of N-terminal proB-type natriuretic peptide, remarkably improve pathological changes of heart tissues of model rats, regulate and control the heart functions of the model rats, improve the systolic function of the heart, relieve expression of inflammatory factors such as interleukin-1beta, interleukin-6 and tumor necrosis factor-alpha of the rats and improve the anti-inflammatory effect of the rats. The action mechanism of the compound relates to a plurality of pathways such as extracellular matrix receptor interaction, a chemotactic factor signal pathway, a relaxin signal pathway, a cyclic adenosine monophosphate signal pathway, a nuclear factor-kB signal pathway, fatty acid metabolism and a Toll-like receptor signal pathway, and the compound is an effective medicament for treating ischemic heart failure.

The present invention relates a process for preparing a compound of Formula XX wherein: R1 is hydrogen, optionally substituted alkyl, alkenyl, alkynyl, cycloalkyl, aryl, heterocyclyl, heteroaryl, aralkyl, alkoxy, aryloxy, alkenyloxy or alkynyloxy; R2 is an N-containign heterocyclyl or heteroaryl; and Q is optionally substitued aryl or heteroaryl. Furthermore a compound of the present invention are useful in the treamtment of various inflammatory, autoimmune and allergic diseases, such as method of treating asthma, rheumatoid arthritis, COPD, rhinitis, osteoartluitis, psoriatic arthritis, psoriasis, pulmonary fibrosis, wound healing disorders, pulmonary inflammation, acute respiratory distress syndrome, perodontitis, multiple sclerosis, gingivitis, atherosclerosis, neointimal proliferation, which leads to restenosis and ischemic heart failure, stroke, renal diseases, tumor metastasis, and other inflammatory disorders characterized by the overexpression and over-activation of a matrix metalloproteinase using the compound.

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 discloses application of sFRP2 in preparation of a medicine for treating ischemic heart failure by inhibiting a Wnt / beta-catenin signal channel, a related kit and a medicine screening method, relates to the technical field of biological medicines, and discloses application of sFRP2 in preparation of a medicine for treating heart failure caused by ischemic cardiomyopathy by inhibiting the Wnt / beta-catenin signal channel. The medicine comprises an effective dose of sFRP2 protein; the medicine is characterized by comprising a Wnt / beta-catenin signal channel inhibitor, the invention relates to a kit for evaluating the risk of ischemic heart failure. The kit comprises a reagent for detecting the expression level of sFRP2 and Wnt / beta-catenin; the invention relates to an application in a medicine for treating ischemic heart failure by inhibiting a Wnt / beta-catenin signal channel, a related kit and a medicine screening method, which are used for developing a new treatment medicine and improving the treatment effect of the ischemic heart failure. Meanwhile, the invention provides a kit for evaluating the risk of ischemic heart failure, and early and accurate diagnosis and risk evaluation of the disease are realized.

The present invention relates to the use of a pharmaceutically effective amount of an short-acting calcium channel blocking compound to treat ischemic heart conditions, cardiac arrhythmias, hypertensive crisis in an emergency room setting, hypertension before, during, or after surgery, no-reflow phenomenon following reperfusion, and diseases associated with decreased skeletal muscle blood flow. The invention also relates to pharmaceutical compositions formulated for use in such methods and to kits for such methods.

The present invention relates to B-hydroxy and amino substituted carboxylic acide, which act as matrix metalloprotease inhibitor, particularly diastereomerically pure B-hydroxy carboxylic acid, corresponding processes for the synthesis of and pharmaceutical composition containing the compounds of the present invention. Compound of the present invention are useful in the treatment of various inflammatory, autoimmune and allergic diseases, such as methods of treating asthma, rheumatoid arthritis, COPD, rhinitis, osteoarthritis, psoriatic arthritis, psoriaasis, pulmonary fibrosis, wound healing disorders, pulmonary inflammation, acute respiratory distress syndrome, perodontitis, multiple sclerosis, gingivitis, atherosclerosis, neointimal proliferation, which leads to restenosis and ischemic heart failure, stroke, renal diseases, tumor metastasis, and other inflammatory disorders characterized by the over-expression and over-activation of a matrix metalloproteinase using the compound.

An interventional ostium occlusion catheter includes a catheter tube with at least one port at a first end, a tip at a second end, and a central lumen, with a positioning component and an occlusion component on the surface of the catheter tube close to the tip. A method of coronary intervention using the catheter includes maneuvering the catheter to an ostium; inserting the catheter into a coronary vessel; activating the positioning component and the occlusion component; and delivering an infusion via the lumen. An interventional system for improving management of ischemic cardiac tissue during acute coronary syndromes includes the catheter; a blood infusion device that delivers controlled reperfusate; and a ventricular unloading device that manipulates myocardial oxygen demand in a coronary chamber. The operator can mitigate reperfusion-related and oxygen-related tissue injury by precisely modulating oxygen re-exposure when re-establishing flow and when using a ventricular unloading device.

The present application relates to a kind of traditional Chinese medicine composition for treating ischemic heart failure and preparation method thereof, belong to the field of traditional Chinese medicine pharmacy, the traditional Chinese medicine composition includes: cassia 5-15 parts, white atractylodes 5-15 parts, poria 5-15 parts, dried ginger 6-12 parts, acanthopanax 5-15 parts, water red flower seed 10-30 parts, verbena 3-9 parts, dogwood 6-12 parts, fried licorice 3-9 parts.The composition can significantly reduce N-terminal B-type natriuretic peptide level, significantly improve model rat heart tissue pathological changes, regulate the heart function of model rat, improve the systolic function of heart, and can reduce the expression of rat interleukin-1 beta, interleukin-6, tumor necrosis factor-alpha and other inflammatory factors, involve extracellular matrix receptor interaction, chemotactic factor signal pathway, relaxin signal pathway, cyclic adenosine monophosphate signal pathway, nuclear factor-kappa B signal pathway and multiple pathways, and is effective drug for treating ischemic heart failure.

Disclosed in the present invention is a novel method for investigating a mechanism of pericyte‑to‑fibroblast transition in ischemic heart failure, comprising the following steps: S1, sample preparation; S2, single-cell expression matrix construction; S3, cell quality control; S4, cell type annotation; S5, cell subtype annotation; S6, cell metabolism analysis; S7, cell differentiation trajectory analysis; and S8, cell-cell communication analysis. Single-cell sequencing is performed on hearts of healthy mice and IHF mice, pericytes and fibroblasts are identified from cardiac transcriptional profiles of the healthy mice and the IHF mice, and then potential differences in cell-cell interaction signals are investigated; moreover, core regulatory factors that cause dysfunction in pericyte signal communication are revealed, providing potential therapeutic targets for the treatment of ischemic heart failure. Rarres2 and Tnfsf12 genes can serve as therapeutic targets for the treatment of myocardial fibrosis in ischemic heart failure.

The application discloses an animal model construction method simulating human ischemic heart failure, and relates to the field of biomedical experimental animal models, and comprises the following steps: S1, model construction: embolism suspension liquid containing microspheres with a specific diameter is injected into the left ventricular cavity of a target animal through percutaneous puncture, so that the microspheres are embolized in myocardial microvessels through coronary artery circulation, thereby establishing a coronary artery microembolism model; S2, early screening: within 24 hours after model construction, cardiac ultrasound detection and serum biomarker detection are performed on the target animal; the animal model construction method simulating human ischemic heart failure simulates embolism of human myocardial arterioles and capillary arterioles by controlling the particle size (15-45 mu m) of the microspheres, induces diffuse myocardial ischemia closer to the clinic, thereby stably leading to progressive ventricular remodeling and chronic heart failure, rather than acute transmural infarction.