6 results about "Rat myocardium" patented technology

The invention discloses an NLRP3 inhibitor as well as a preparation method and application thereof. Specifically, the invention relates to a compound shown as a formula (NLRP3i-3) or a pharmaceutically acceptable salt thereof, the formula (I) is COCCNc1nc2c (c (= O) n (C) c (= O) n2C) n1Cc1cc (OC) ccc1N, and the chemical name is 8-((4-amino-2-methoxybenzyl)-7, 9-dimethyl-7, 9-dihydro-8H-purine-6, 8-diketone. The invention also provides a preparation method of the compound, a pharmaceutical composition containing the compound, and application of the compound in preparation of drugs for preventing and / or treating NLRP3-mediated diseases. The disease is preferably myocardial ischemia reperfusion injury. Experimental results show that the compound provided by the invention has excellent NLRP3 inhibitory activity (IC50lt, 100nM), and has high selectivity to NLRP3 inflammasomes; good pharmacokinetic characteristics are achieved in a rat body, and the bioavailability is high; in myocardial ischemia reperfusion injury models of mice and rats, the composition can significantly reduce myocardial infarction area, reduce myocardial enzyme level, alleviate inflammatory response and improve heart function; preliminary toxicological evaluation shows that the safety is good. Therefore, the compound disclosed by the invention is expected to be developed into a novel medicine for treating NLRP3 related diseases such as myocardial ischemia-reperfusion injury.

The application relates to application of siRNA-OTUB1 in preparation of drugs for preventing or treating myocardial cell hypertrophy, and belongs to the biomedical technical field.The nucleotide sequence of the OTUB1 gene is shown as SEQ ID NO.1, and the targeted nucleotide sequence of the siRNA-OTUB1 for specifically interfering with the expression of the OTUB1 gene is shown as SEQ ID NO.2 or SEQ ID NO.3.The application innovatively proposes a strategy for preventing or treating myocardial cell hypertrophy by taking deubiquitinase OTUB1 as a core target point and by interfering with the expression thereof.In a myocardial cell experiment of a milk rat, the application of the designed siRNA-OTUB1 can effectively reduce the expression levels of OTUB1 mRNA and OTUB1 protein, and further reduce the degree of myocardial cell hypertrophy.Based on the finding, the OTUB1 gene can be developed as a novel treatment target point for myocardial cell hypertrophy, is used for designing a targeted drug, and provides a new technical thought for precise treatment of myocardial hypertrophy.

The application belongs to the technical field of medicine, and particularly relates to application of acacetin or 6-hydroxyflavone in preparation of anti-angina pectoris drugs, and aims to solve the problems of adverse reactions such as blood pressure drop, reflex tachycardia and the like caused by non-selective vasodilation of existing anti-angina pectoris drugs, wherein the drug improves myocardial blood supply by selectively dilating coronary vessels of the heart, wherein acacetin dilates coronary vessels of the heart by inhibiting cardiac coronary vessel myosin light chain kinase and activating myosin light chain phosphatase, and 6-hydroxyflavone dilates coronary vessels of the heart by inhibiting protein kinase C and enhancing myosin light chain phosphatase activity; and the acacetin or 6-hydroxyflavone significantly reduces the symptoms of myocardial ischemia of rats caused by isopropyl adrenaline, improves characteristic ECG abnormal changes of angina pectoris, does not affect heart rate and systemic blood pressure, and is safer, thereby providing a potential drug selection for anti-angina pectoris treatment.

The invention relates to application of siRNA-OTUB1 in preparation of a medicine for preventing or treating myocardial cell hypertrophy, and belongs to the technical field of biomedicine. The nucleotide sequence of the OTUB1 gene is as shown in SEQ ID NO.1, and the target nucleotide sequence of the siRNA-OTUB1 for specifically interfering with the expression of the OTUB1 gene is as shown in SEQ ID NO.2 or SEQ ID NO.3. The invention further discloses the application of the siRNA-OTUB1 gene. The invention innovatively provides a strategy for preventing or treating myocardial cell hypertrophy by intervening the expression of the deubiquitinating enzyme OTUB1 serving as a core target. In a myocardial cell experiment of a milk rat, by applying the siRNA-OTUB1 designed by the invention, the expression level of OTUB1 mRNA and OTUB1 protein can be effectively reduced, so that the hypertrophy degree of myocardial cells is reduced. Based on the discovery, the OTUB1 gene can be developed into a novel therapeutic target for myocardial hypertrophy, is used for designing targeted drugs, and provides a new technical thought for precise treatment of myocardial hypertrophy.

The application belongs to the technical field of biological medicine, and particularly relates to a biomarker and application thereof. The application finds that the expression level of a specific subtype of a nicotine acetylcholine receptor of an arrhythmia patient is significantly lower than that of a sinus rhythm population, and the expression of the nicotine acetylcholine receptor in ischemia / reperfusion injury myocardium of a rat and myocardium of a heart failure patient also shows a significant downward trend. Further research finds that the expression loss of the specific subtype of the nAChR significantly increases the risk of arrhythmia. In combination with animal experiment results and human clinical data, it can be seen that the expression defect of the endogenous cholinergic system is closely related to fatal arrhythmia.

The invention belongs to the technical field of biology, and discloses an engineering mesenchymal stem cell transformation method based on cholesterol anchoring and antibody modification and application of the engineering mesenchymal stem cell transformation method. The rigidity of the cell membrane of the MSCs is reduced by regulating and controlling the cholesterol level on the cell membrane, and the MSCs are promoted to pass through narrow capillaries with higher deformation capacity, so that the non-specific aggregation in the lung is reduced. Besides, exogenous modified cholesterol is used as an anchor point on a cell membrane, specific antibodies aiming at different damaged tissues are modified on the surfaces of the MSCs by means of DNA self-assembly, and the engineered MSCs are constructed. Experimental results show that in a mouse acute kidney injury and colitis model and a rat myocardial infarction model with higher blood flow shearing force, the engineered MSCs for modifying cholesterol and a specific antibody can reduce retention in the lung and improve homing efficiency of damaged tissues.