15 results about "Reperfusion Damages" patented technology

This invention discloses a micropeptide, its encoding nucleic acid, and its application in regulating inflammatory activation of microglia. The amino acid sequence of the micropeptide is shown in SEQ ID NO:3. Simultaneously, this invention discloses the nucleic acid encoding the micropeptide, which contains either the nucleotide sequence shown in SEQ ID NO:1 or the nucleotide sequence shown in SEQ ID NO:2, wherein SEQ ID NO:2 is a small open reading frame located within the sequence of SEQ ID NO:1. This invention validated the translational expression of the micropeptide in microglia by constructing an EGFP reporter gene fusion vector and a SUMO tag fusion expression vector. Functional experiments showed that under oxygen-glucose deprivation / reperfusion injury conditions, the micropeptide significantly inhibited inflammatory activation of microglia. This invention provides a new potential target and candidate drug for the treatment of neuroinflammatory diseases such as stroke.

Compounds, compositions and methods for improving the viability and / or function of cells or for the in vitro, ex vivo or in vivo protection of cells, tissue, graft or organs from various damages are described. The reagents and composition are based on activation of the heat shock response activation and / or the antioxidant response and include for example. HSP90 co-factor inhibitor such as Celastrol or Celastrol analogs used alone or in combination with an adjunct agent (e.g., a NRF-2 activator, antioxidant, etc.). Therapeutic enhancement may also include increase in paracrine effector production and signaling. Methods for improving the resistance of cells, tissue, grafts or organs to damages or stress, such as hypoxic or oxidative stress-induced cell death, and / or for improving the viability and retention of transplanted or transfused cells are also described. Therapeutic treatment or prevention of ischemic injury (e.g. myocardial infarct, ischemia / reperfusion injury) and related stressors (hypoxia, oxidative stress, inflammation, sepsis / shock, etc) are also provided.

The application relates to application of miRNA and / or a miRNA agonist in preparation of a medicine for preventing and / or treating myocardial ischemia-reperfusion injury, and belongs to the technical field of biological medicine. The medicine is administered through skeletal muscle injection, is secreted to a circulation system after expression on the skeletal muscle, is delivered to heart tissue by taking extracellular vesicles as carriers, and thus regulates myocardial cell functions. According to the animal model verification result, the miRNA can be delivered to the heart by the extracellular vesicles secreted by the skeletal muscle through injection of the medicine into the skeletal muscle, the expression level of the miRNA in the I / RI heart is significantly increased, the myocardial infarction area is effectively reduced, myocardial cell apoptosis is inhibited, myocardial fibrosis is reduced, and heart function is improved, a brand-new intervention strategy is provided for treatment of myocardial ischemia-reperfusion injury and related heart diseases, and a brand-new idea is opened up for research and development of heart failure treatment medicines.

This invention discloses the application of HY-Q67280 in the preparation of drugs for the prevention and / or treatment of myocardial ischemia / reperfusion injury, belonging to the field of biomedical technology. HY-Q67280 can activate the E3 ubiquitin ligase MARCH9. MARCH9 inhibits Drp1-dependent mitochondrial dysfunction, oxidative stress, and ferroptosis by targeting FXR1 degradation, reducing apoptosis and mitochondrial oxidative stress levels in mouse myocardial ischemia / reperfusion and rat neonatal primary cardiomyocytes after hypoxia / reoxygenation, and reducing mitochondrial division to improve mitochondrial function, thereby protecting against myocardial ischemia / reperfusion injury.

The present disclosure provides compounds of formula 1 to inhibit or prevent mitochondrial dysfunction by augmenting mitochondrial function. Mitochondrial dysfunction is the hallmark of a wide range of diseases and disorders. Mitochondria are a promising therapeutic target for the detection, prevention and treatment of various human diseases such as cancer, neurodegenerative diseases, ischemia-reperfusion injury, diabetes and obesity.

The invention provides methods of treating ischemia / reperfusion injury in a subject. In one example, a method comprises administering a therapeutically effective amount of a pharmaceutical composition that increases levels of Bcl2-associated athanogene 3 (BAG3) polypeptide in ischemic tissue. The invention also provides methods of treating a subject at risk of ischemia / reperfusion injury. In one example, a method comprises administering a therapeutically effective amount of a pharmaceutical composition that increases levels of Bcl2-associated athanogene 3 (BAG3) polypeptide. In the invention methods, in one example, a pharmaceutical composition comprises a nucleic acid encoding BAG3 polypeptide.

The application belongs to the technical field of biomedicine, and particularly relates to application of circRNA_0004468 in a drug for treating ischemic stroke. The application first discloses and verifies a competitive endogenous RNA (ceRNA) regulatory axis composed of circRNA_0004468, miR-1224 and VEGFA, which is a key molecular mechanism for RIPostC to play a neuroprotective role. Experiments prove that circRNA_0004468 can adsorb miR-1224 as a "molecular sponge", thereby relieving the inhibition of miR-1224 on VEGFA, up-regulating the expression of VEGFA, and then activating the PI3K / AKT signaling pathway and promoting angiogenesis, so as to finally reduce ischemia / reperfusion injury at the cell (OGD / R model) and animal (tMCAO model) levels.

This invention relates to a drug for treating ischemia-reperfusion injury and its application. The drug activates the CCL2-chemokine receptor 2 signaling axis, triggering the downstream G protein αi2 subunit-mediated phosphatidylinositol 3-kinase / protein kinase B signaling pathway. This, in turn, synergistically regulates the antioxidant defense system driven by nuclear factor erythroid 2-related factor 2 and the B-cell lymphoma 2-mediated anti-apoptotic pathway, thereby treating the ischemia-reperfusion injury. The results of this study establish a novel therapeutic strategy for testicular ischemia-reperfusion injury based on engineered exosomes, and simultaneously reveal the previously undiscovered cytoprotective role of the CCL2 / CCR2 signaling axis in non-immune cells.

This invention provides a modeling device and method for simulating myocardial ischemia-reperfusion injury in an isolated heart, applicable to the field of data processing. This application aims to model ischemia-reperfusion injury in an isolated heart. First, it collects multi-source core data, including samples, perfusion data, environmental data, and physiological monitoring. Utilizing an isothermal perfusion and oxygen partial pressure regulation system, it completes cardiac rewarming, cannulation, and stable perfusion, simultaneously monitoring key indicators such as heart rate, coronary blood flow, and ventricular pressure. Ischemia and reperfusion parameters are integrated to form a basic perfusion dataset. The dataset is hierarchically structured according to physiological indicators and environmental parameters, constructing ternary association nodes for samples, indicators, and parameters. A dynamic physiological association graph is generated through temporal matching and aggregation. Core features are extracted through injury assessment and temporal prediction, generating high-dimensional vectors. These vectors are imported into an adaptive engine for iterative optimization, combined with deviation visualization to form a basic modeling model, outputting modeling information applicable to simulating ischemia-reperfusion injury in an isolated heart.

This invention discloses an injury-related endogenous polypeptide and its applications. The invention employs a "single-model initial screening – multi-model cross-validation" strategy, using an acute lung injury (ALI) model as the screening set and partial hepatectomy (PHx) and cerebral ischemia-reperfusion injury (tMCAO) models as the validation set. Combined with liquid chromatography-tandem mass spectrometry (LC-MS / MS) technology, a group of serum endogenous polypeptides was screened. These polypeptides are novel epitope fragments generated by specific enzymatic digestion of precursor proteins such as fibrinogen α-chain and hemoglobin α / β subunits in the tissue injury microenvironment. Their expression levels are extremely low in healthy serum but exhibit explosive upregulation in injured states. Experiments have confirmed that this group of polypeptides shows significant responses in acute lung injury, liver injury, and cerebral ischemia-reperfusion injury models, and can serve as broad-spectrum biomarkers for multi-tissue injury, providing a novel detection target for the early diagnosis of multi-tissue injury in acute and critical clinical settings.

This invention discloses the application of PAFAH2 protein in the preparation of products for the prevention and / or treatment of ischemia-reperfusion injury. This invention reveals for the first time that platelet-activating factor and its phospholipid-like components can induce ferroptosis in cells. On the one hand, they can directly increase cell membrane permeability; on the other hand, they can be secreted extracellularly, acting as propagation factors for ferroptosis and promoting its spread within the cell population. PAFAH2, as an intracellular specific hydrolase against platelet-activating factor and its phospholipid-like components, resists ferroptosis by scavenging these oxidative substrates. Ischemia-reperfusion leads to ferroptosis in tissue cells. This invention, through the injection of human recombinant PAFAH2 protein, removes oxidatively truncated phospholipids generated during reperfusion, thereby protecting tissue cells from the occurrence and spread of ferroptosis caused by lipid peroxidation and inhibiting large-area tissue damage caused by ischemia-reperfusion.

The application discloses application of norisoboldine or a pharmaceutically acceptable salt, a polymorph or a solvate thereof in preparation of a drug for preventing or treating myocardial ischemia-reperfusion injury. It is found that the compound can rapidly target ischemia-reperfusion damaged myocardial cells, inhibit ROS / MDA oxidative stress, quench inflammation storm, and reversely change mitochondrial membrane potential collapse, down-regulate pro-apoptotic protein Bax and up-regulate anti-apoptotic protein Bcl-2, and then inhibit Caspase 3 cleavage, thereby effectively blocking a lethal apoptosis network of myocardial cells from the source. The drug can significantly improve the survival rate of myocardial cells and reduce the myocardial infarction area, and provides a multi-target, mechanism clear new candidate drug for clinical prevention and treatment of acute cardiovascular critical illness.

The application relates to the technical field of kidney treatment, and particularly discloses a method for extracting emodin and application of the emodin in renal ischemia-reperfusion injury. The method comprises the following steps: S1, crushing traditional Chinese medicine rhubarb raw materials to obtain traditional Chinese medicine rhubarb powder; S2, mixing the traditional Chinese medicine rhubarb powder with ethanol and performing ultrasonic treatment to obtain a primary extraction solution; S3, adding cellulase to the primary extraction solution to obtain an enzymatic solution; S4, performing supercritical CO2 extraction on the enzymatic solution, and collecting an extraction phase; S5, adding ethyl acetate to the extraction phase for extraction, and then separating an organic phase; S6, crystallizing the organic phase, and filtering to obtain emodin crude products; and S7, recrystallizing the emodin crude products with methanol, and drying to obtain finished products. The method for extracting emodin can be used for preparing medicines for treating kidney diseases, in particular, renal ischemia-reperfusion injury, and has the advantages of high extraction efficiency, high product purity and a green and environment-friendly process.

The present application provides the use of aucubin or the combination of aucubin and ACA in the preparation of a medicament for treating ischemic brain injury, in particular acute cerebral ischemia-reperfusion injury. The present application first discovers that aucubin or the combination of aucubin and ACA can increase the blood flow of the ischemic side after ischemic brain injury in mice; significantly reduce the cerebral infarction volume; improve the cognitive and motor function of mice after ischemic brain injury; reduce the degree of injury caused by cerebral ischemia, significantly improve the degree of neuronal necrosis of brain tissue after ischemia; significantly increase the survival rate of HT22 cells after oxygen-glucose deprivation and reperfusion injury, reduce intracellular Ca 2+ fluorescence intensity, and inhibit cell apoptosis.

The application provides application of a myocardial peptide in ischemia-reperfusion injury drugs after myocardial infarction intervention, and belongs to the technical field of biological medicine. The application provides a preparation method of the myocardial peptide. The myocardial peptide polypeptide prepared through sound wave treatment and electrolysis treatment has higher polypeptide content and small molecule polypeptide ratio, higher yield, and a simplified process. The myocardial peptide provided by the application can improve the heart function of STEMI patients treated by PCI, reduce the myocardial infarction area, and can be used for preparing drugs for treating myocardial infarction.