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42 results about "Myocardial apoptosis" patented technology

Myocardial apoptosis mediated by mitochondrial dysfunction is an important mechanism for the initiation and progression of heart failure. MiRNAs act as negative regulators of gene expression and play a vital role in the development of heart failure.

MiRNA-140 inhibitor and applications thereof

The invention provides a miRNA-140 inhibitor and applications thereof, wherein a sequence of the inhibitor has at least 90% of homology with a nucleotide sequence showing in the following SEQ ID NO:1: 5'-CUACCAUAGGGUAAAACCACUG-3', wherein each basic group is modified by 2'-O-methyl; and the miRNA-140 inhibitor is used for preparing a medicament or a kit for diagnosing, preventing, treating and / or prognostically evaluating heart diseases. The miRNA-140 inhibitor is changed in treatment of myocardial ischemia injury and myocardial apoptosis and has a myocardial preservation effect.
Owner:INST OF ZOOLOGY CHINESE ACAD OF SCI

Application of a human amniotic mesenchymal stem cell

ActiveCN105769910BImproved flow dynamicsProtect against pathological changesUnknown materialsSkeletal/connective tissue cellsCardiac functioningAcyl CoA dehydrogenase
The invention discloses application of human amniotic mesenchymal stem cells in preparation of a preparation for treating a myocardial ischemia reperfusion injury generated after cardiopulmonary bypass.In the myocardial ischemia reperfusion process after the cardiopulmonary bypass, the human amniotic mesenchymal stem cells can effectively prevent myocardial cells from being injured in myocardial ischemia reperfusion, obviously improve the cardiac functions, lower the levels of myocardial injury specific marker protein lactic dehydrogenase, creatine kinase isoenzyme and troponin I, lower the levels of a plasma inflammatory factor interleukin-8 and a tumor mecrosis factor-alpha, increase the content of the plasma inflammatory factor interleukin-10, obviously improve pathological changes of the myocardial tissue, reduce myocardial cell apoptosis, lower the expression level of cell apoptosis promoting protein, increase the expression quantity of anti-apoptoasis protein and can protect the functions of myocardial cell mitochondria.By preparing the human amniotic mesenchymal stem cells into an injection for treatment on the myocardial ischemia reperfusion injury generated after the cardiopulmonary bypass, the cardiac functions can be effectively protected, and postoperative complications of the cardiopulmonary bypass are relieved.
Owner:AFFILIATED HOSPITAL OF ZUNYI MEDICAL COLLEGE

Application of MST1 gene in detecting and/or regulating excessive apoptosis of myocardial cells

The invention belongs to the field of molecular biology, and provides a preparation for detecting myocardial cell excessive apoptosis and a method for detecting myocardial cell excessive apoptosis. The invention also provides an application of the MST1 gene expression plasmid in preparation of a preparation for improving the myocardial cell apoptosis rate in a high-glucose environment, an application of the siRNA interference plasmid of the MST1 gene in preparation of a preparation for reducing the myocardial cell apoptosis rate in the high-glucose environment, and a method for regulating andcontrolling the myocardial cell apoptosis rate. By utilizing the relationship between the MST1 gene and myocardial cell excessive apoptosis, especially myocardial cell excessive apoptosis in a high-glucose environment, the preparation for detecting myocardial cell excessive apoptosis provided by the invention can be used for efficiently and accurately detecting the apoptosis condition of myocardial cells in the high-glucose environment; and therefore, whether excessive apoptosis occurs to cardiac muscle cells cultured in vitro or development of heart tissue during fetal development in a motherbody or not is accurately judged.
Owner:国家卫生健康委科学技术研究所

Method for attacking miRNAs through free radicals to cause oxidative damage to RNAs

The invention relates to a method for attacking miRNAs through free radicals to cause oxidative damage to the RNAs. According to the method, 8-oxoguanine is generated through oxidation of guanine 8-bit carbon in an oxidative stress state so that the miRNAs undergo oxidative damage. A damage mode is selected from one or more of the following modes: (1) the oxidative damage is caused to the miRNAs through a Fenton reagent oxidation system; (2) the oxidative damage is caused to the miRNAs in the process of using H2O2 to process and induce apoptosis; (3) the oxidative damage is caused to the miRNAs in a Fe overloading induced myocardial injury animal model; and (4) the oxidative damage is caused to the miRNAs in a myocardial ischemia-reperfusion injury animal model. According to the method, the miRNA subtype variety of the miRNAs undergoing the oxidative damage in the process of using H2O2 to induce the myocardial apoptosis is determined, and functional differences are expressed through the generation and degradation of the oxidative damage miRNAs in myocardial cells, location characteristics, the synergistic effect with other biomacromolecule and oxidative damage miRNA regulatory genes. The method is simple in process and obvious in damage effect, the applied range is wide, and the method has application environment friendliness.
Owner:QINGDAO UNIV
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