8results about How to "Reduce fibrosis" patented technology

The invention relates to application of tsRNA-3025a as a prognostic marker of acute myocardial infarction and a treatment target spot of myocardial ischemia reperfusion injury. A DNA (Deoxyribonucleic Acid) sequence corresponding to the tsRNA-3025a is shown as SEQ ID NO: 1: 5 '-ATCCTGCCGACTACGCCA-3'. The tsRNA-3025a can be used for treating acute myocardial infarction and myocardial ischemia reperfusion injury. In the aspect of prognosis, a detection kit is provided, and the risk of heart failure and short-term adverse events of a patient is evaluated by quantitatively detecting the expression level of the tsRNA. In the aspect of treatment, the invention provides the application of the anti-tagomir for inhibiting the function or expression of tsRNA-3025a in the preparation of the medicine for treating the myocardial ischemia reperfusion injury, and the anti-tagomir is subjected to specific chemical modification. A novel biomarker is provided for prognosis risk stratification of acute myocardial infarction, and an effective treatment strategy is provided for prevention and treatment of myocardial ischemia-reperfusion injury.

The invention discloses application of triflorin or pharmaceutically acceptable salt or solvate thereof in preparation of a medicine for preventing, delaying and / or treating heart aging and / or myocardial injury. The invention provides a new strategy and a candidate substance for developing medicines, health-care products or functional foods for preventing, delaying and / or treating heart aging and / or myocardial injury, maintaining heart health and reducing the risk of aging-related cardiovascular diseases.

The application discloses application of an Hsc70 inhibitor in preparation of a medicine for treating ischemic heart disease, and belongs to the technical field of medicines for treating ischemic heart disease. The application proves through pharmacodynamics and molecular mechanism research that a specific small-molecule inhibitor of Hsc70 can be used for preparing a medicine for treating ischemic heart disease or myocardial regeneration. The specific small-molecule inhibitor of Hsc70 directly combines with an ATP enzyme domain of Hsc70, blocks the interaction between Hsc70 and mitochondrial fusion protein 2 (Mfn2), further reduces the contact between mitochondria and lipid droplets under pathological conditions, and then releases cell cycle inhibition and up-regulates CDK1 and MCM5 expression. The medicine can significantly reduce the infarction area after myocardial infarction, reduce fibrosis, improve the systolic and diastolic functions of the heart, and can protect myocardial cells from suffering from hypoxia / reoxygenation-induced systolic dysfunction, thereby providing a new medicine selection for clinically treating myocardial infarction and heart failure.

This invention discloses a vitamin A-functionalized polyphenol-phospholipid complex, its preparation method, and its applications, belonging to the field of pharmaceutical formulation and nanodelivery technology. The phospholipid complex comprises a polyphenol drug, a phospholipid material, and a vitamin A phospholipid ligand. The vitamin A phospholipid ligand is formed by vitamin A or its derivatives and a phospholipid derivative containing amino or other reactive groups. The phospholipid complex forms a phospholipid composite structure through non-covalent interactions between the polyphenol drug and the phospholipid material, and the vitamin A phospholipid ligand is inserted into or assembled into the surface or interior of the phospholipid composite structure. Animal experiments show that this phospholipid complex can reduce serum transaminase levels and alleviate the degree of liver fibrosis, and has good blood compatibility and tissue safety. This invention provides an industrially achievable targeted nano-formulation solution for early intervention in liver fibrosis, with promising application prospects.

The invention relates to hydrogel as well as a preparation method and application thereof, and belongs to the technical field of biological hydrogel materials. The hydrogel comprises a prednisolone sodium phosphate hydrogel P-Gel skeleton and gold nanoparticles PCAu, wherein the gold nanoparticles PCAu are uniformly loaded on the P-Gel skeleton and are coated by procyanidine. According to the preparation method, a three-dimensional cross-linked network skeleton of PSP hydrogel P-Gel is self-assembled and constructed by utilizing ion coordination and hydrogen-bond interaction of prednisolone sodium phosphate PSP under the action of Ca < 2 + >, and the hydrogel PCAu-coated P-Gel is formed by uniformly loading gold nanoparticles PCAu which are green synthesized from procyanidine PC and have stable surfaces. The hydrogel can promote rapid repair of spinal cord injury and relieve far-end muscle atrophy and fibrosis; and meanwhile, the injectable self-healing hydrogel has the engineering advantages of injectability, self-healing and the like, and shows good clinical transformation potential.

The invention discloses a fusion polypeptide RAT-1 and application thereof in hypertension treatment. The topological structure of the fusion polypeptide is a kidney targeting head-ACE2 functional segment-MMP responsive connexon-AT1 receptor antagonism segment, and the full-length sequence is as shown in SEQ ID No: 1. The kidney targeting head can be specifically combined with megalin receptors of renal tubular epithelial cells to realize kidney targeting delivery; the ACE2 functional segment can efficiently degrade angiotensin II; the MMP responsive connexon is specifically cut in a focus microenvironment, and an AT1 receptor antagonism segment is released; the AT1 receptor antagonist segment can block the receptor signal channel of angiotensin II. The fusion polypeptide has good plasma stability, shows a powerful and long-acting antihypertensive effect in a spontaneous hypertension rat model, is remarkable in kidney targeting, and can relieve renal fibrosis and protect podocyte functions. The fusion polypeptide disclosed by the invention realizes a synergistic effect of targeted delivery, enzymolysis catalysis, response release and receptor antagonism, and can be used for preparing hypertension treatment medicines and kidney protection medicines.

This invention belongs to the field of regenerative medicine technology, specifically relating to bone marrow-derived macrophages expressing CD301b, TIMD4, and LYVE-1, their preparation method, and applications. The steps are as follows: Primary mouse bone marrow mononuclear precursor cells are cultured in expansion medium for 7 days to obtain macrophages, with the medium changed every 2-3 days during this period; on the 7th day, the expansion medium is replaced with a high-efficiency induction medium and cultured for 46-50 hours to obtain bone marrow-derived macrophages expressing CD301b, TIMD4, and LYVE-1. This invention, through a time-series strategy of TGF-β pre-induction combined with IL-4 / IL-5 / IL-13 synergistic induction, can significantly enhance the expression levels of CD301b, TIMD4, and LYVE-1 in BMDM, making their function close to that of natural cardiac resident macrophages, and effectively exerting anti-inflammatory, repair-promoting, and ventricular remodeling-inhibiting effects after AMI.

The application relates to the field of biological medicine, and provides application of OpiCa1 mutant peptide DE-4A in antagonizing heart failure after myocardial infarction. Experiments prove that the polypeptide DE-4A can remodel myocardial calcium homeostasis by restoring RyR2 protein stability and blocking excessive activation of the CaMKII signal pathway. This mechanism effectively reduces myocardial injury and fibrosis, significantly improves ventricular remodeling and heart dysfunction after myocardial infarction, and provides new experimental evidence for the treatment of ischemic cardiomyopathy. DE-4A has the effects of improving myocardial contractile function, regulating Ca 2+ homeostasis, which may be a key link in the pharmacodynamic mechanism, and provides new experimental evidence for the treatment of ischemic heart disease.