12 results about "Hepatic ischemia" patented technology

Disclosed is a method of treating liver ischemia reperfusion (I / R) injury in a subject. In some aspects, the method comprises providing a subject suffering from liver I / R injury or at risk of suffering liver I / R injury; and administering to the subject one or more heparan sulfate (HS) compounds. In some aspects, the one or more HS compounds comprises about 5 to about 18 saccharide units, optionally about 12 to about 18 saccharide units. In some aspects, the one or more HS compounds comprises about 12 saccharide units.

The invention discloses application of a CGAS-STING signal channel inhibitor in preparation of a medicine for preventing and treating hepatic ischemia-reperfusion injury, and relates to the technical field of biological medicine. According to the application, a cGAS-STING signal channel in macrophages is inhibited by using a cGAS inhibitor or an STING inhibitor, activation of double-stranded deoxyribonucleic acid released by a neutrophile granulocyte extracellular trapping net on a DNA induction channel is blocked, and the M1 type polarization level of the macrophages is reduced. The traditional Chinese medicine composition can effectively relieve liver inflammatory response and cell apoptosis, and a new path is provided for preventing and treating acute liver injury after liver transplantation or liver resection.

This invention belongs to the field of pharmaceutical compound technology, specifically relating to an azafibrone derivative with anti-hepatic ischemia-reperfusion injury activity, its preparation method, and its application. The structural formula of the azafibrone derivative is shown in Formula A: Among them, R 1 For CHO or COOH, R 2 The derivative is H or Cl. This application describes the extraction of an azafibrone derivative from the fermentation broth of *Cryptocaryas* fungi. Experiments have confirmed that this compound possesses anti-hepatic ischemia-reperfusion injury activity, indicating its potential to be developed into an anti-hepatic ischemia-reperfusion injury drug, providing a new option for the development of such drugs.

This invention relates to the field of biomedical materials technology and provides an application of obeticholic acid-exosome nanoparticles in the treatment of hepatic ischemia-reperfusion injury. The obeticholic acid-exosome nanoparticles are prepared by combining exosomes and obeticholic acid using an ultrasonic method, wherein the exosomes are derived from human bone marrow mesenchymal stem cells. The method for preparing the obeticholic acid-exosome nanoparticles is simple and easy to mass-produce. By utilizing exosomes derived from mesenchymal stem cells, the obeticholic acid-exosome nanoparticles improve the drug's targeting in vivo and prolong its circulation time, achieving targeted delivery of obeticholic acid to the liver, thus providing a new targeted therapeutic strategy for hepatic ischemia-reperfusion injury.

The invention discloses application of curcumenone in preparation of a medicine for preventing and treating ischemia-reperfusion injury. The invention proposes and verifies that the caramel curcumenone can be used for preventing and treating the hepatic ischemia reperfusion injury for the first time, and the compound can effectively protect hepatic tissues and avoid liver function damage by inhibiting the oxidative stress level of the hepatic tissues after ischemia reperfusion, avoiding cell ferroptosis and improving bone marrow-derived macrophages, so that the caramel curcumenone can be used for preventing and treating the hepatic ischemia reperfusion injury. The invention provides a novel medicine with great application potential for preventing and treating ischemia reperfusion injury.

The application discloses application of hsa_circ_0003258 in prevention and / or treatment of liver ischemia-reperfusion injury. The application is found by detection that the expression of hsa_circ_0003258 is significantly decreased in liver ischemia-reperfusion patients; overexpression of hsa_circ_0003258 can significantly inhibit macrophage inflammation and the apoptosis level of hepatocytes after hypoxia-reoxygenation treatment, and improve the function of hepatocytes; hsa_circ_0003258 has a protective effect on relieving liver ischemia-reperfusion injury, and has potential to become a drug for treating liver ischemia-reperfusion injury.

The application belongs to the field of biological medicine, and discloses application of echinocystic acid in preparation of a medicine for preventing and treating liver ischemia-reperfusion injury. The application proves that the echinocystic acid significantly improves liver tissue injury, reduces serum ALT and AST levels, and reduces cell apoptosis through a mouse liver IRI model. It is found that the echinocystic acid activates the p38 MAPK signal pathway by inhibiting PTPN1, thereby activating Nrf2 and enhancing PINK1 / Parkin-mediated mitochondrial autophagy. In addition, the echinocystic acid promotes DRP1 phosphorylation and enhances the transfer of DRP1 to mitochondria, thereby reducing oxidative stress and inflammatory response. It is shown that the echinocystic acid regulates mitochondrial autophagy through the PTPN1 / p38 MAPK / Nrf2 pathway, has a significant liver protection effect, and provides a new idea for the treatment of IRI.

The application discloses a biomarker of liver ischemia-reperfusion injury based on proteomics, and the biomarker is neutrophil granule protein (NGP), which can be used for early diagnosis and prevention of post-hepatectomy complications, prognosis monitoring and judgment, etc.

This invention discloses a method for modifying lipid vesicles with an amphiphilic polymer containing N-oxide teramine groups. The amphiphilic polymer is OPDEA-PCL. OPDEA-PCL is used to modify synthetic liposomes, yielding amphiphilic polymer-synthetic liposome nanoparticles. OPDEA-PCL is also used to modify natural exosomes, yielding amphiphilic polymer-exosome nanoparticles. The amphiphilic polymer-synthetic liposomes of this invention possess active liver and lung targeting functions. This invention, through the engineered modification of exosomes with OPDEA-PCL, accurately guides exosomes to the liver regions requiring treatment, thereby enhancing the repair effect of exosomes on liver ischemia-reperfusion injury.

The present application relates to a nucleic acid molecule comprising a first nucleic acid sequence comprising at least a portion of a 5′ untranslated region (5′ UTR) of a carboxylesterase gene and a second nucleic acid sequence encoding a protein of interest, where the second nucleic acid sequence is heterologous to and operatively coupled to the first nucleic acid sequence. Also disclosed are methods of expressing a protein of interest in a target cell, methods of treating subject for cardiac ischemia or hepatic ischemia, and methods of identifying a nucleic acid sequence capable of selectively enhancing translation of a heterologous protein of interest in a target cell.

The invention belongs to the technical field of biological medicines, and particularly relates to application of an inhibitor targeting an Hnf4 alpha os gene in liver macrophages in preparation of a medicine for preventing and treating liver ischemia-reperfusion injury. According to the application disclosed by the invention, the Hnf4 alpha os gene in the targeted liver macrophage is specifically knocked down or knocked out, so that the expression of the Hnf4 alpha os gene is inhibited, and the injury of a liver ischemia-reperfusion injury model can be remarkably improved; the reagent (an inhibitor of the Hnf4 alpha os gene in the targeted liver macrophage) for specifically knocking down or knocking out the Hnf4 alpha os gene in the targeted liver macrophage can be applied to preparation of the medicine for preventing and treating the hepatic ischemia reperfusion injury.

The use of 2,6-DMHQ in ischemia-reperfusion-related injuries, preferably against cardiac and hepatic ischemia-reperfusion injuries. 2,6-DMHQ can reduce serum ALT and AST and ameliorate liver necrosis. 2,6-DMHQ can also reduce the cardiac enzyme profile, including CK, CK / MB and LDH, and reduce myocardial infarct size.