39 results about "Kidney ischemia" patented technology

A method and kit for detecting the immediate or early onset of renal disease and injury, including renal tubular cell injury, utilizing NGAL as an immediate or early on-set biomarker in a sample of blood serum. NGAL is a small secreted polypeptide that is protease resistant and consequently readily detected in the blood serum following renal tubule cell injury. NGAL protein expression is detected predominantly in proximal tubule cells, in a punctuate cytoplasmic distribution reminiscent of a secreted protein. The appearance NGAL in the serum is related to the dose and duration of renal ischemia and nephrotoxemia, and is diagnostic of renal tubule cell injury and renal failure. NGAL detection is also a useful marker for monitoring the nephrotoxic side effects of drugs or other therapeutic agents.

The present invention encompasses the use of compounds for a novel approach to treat and prevent diseases, conditions, and disorders such as diabetes and ischemic reperfusion injury. Compounds of the invention, including but not limited to BAM15 ((2-fluorophenyl){6-[(2-fluorophenyl)amino](1,2,5-oxadiazolo[3,4-e]pyrazin-5-yl)}amine), a mitochondrial uncoupler, can improve glucose tolerance, increases cellular oxygen consumption, treat or prevent kidney ischemia reperfusion injury reverse insulin resistance, reverse or treat hyperinsulinemia, and reverse or treat hyperlipidemia. The present invention further provides novel compounds as well as methods for identifying compounds with the same or similar properties as BAM15.

The present invention provides a prophylactic or therapeutic agent for a kidney disease, comprising Apoptosis Inhibitor of Macrophage (AIM) or a partial peptide thereof, or a nucleic acid comprising a base sequence encoding the same, or a screening method for a prophylactic or therapeutic agent for a kidney disease, comprising using an animal obtained by subjecting a non-human mammal deficient in AIM expression to unilateral ureteral obstruction or transient kidney ischemia / reperfusion and the like.

The present invention provides a prophylactic or therapeutic agent for a kidney disease, comprising AIM or a partial peptide thereof, or a nucleic acid comprising a base sequence encoding the same, or a screening method for a prophylactic or therapeutic agent for a kidney disease, comprising using an animal obtained by subjecting a non-human mammal deficient in AIM expression to unilateral ureteral obstruction or transient kidney ischemia / reperfusion and the like.

Inflammation is a prominent feature of ischemia-reperfusion injury (IRI) characterized by leukocyte infiltration and renal tubular injury. However, the signals that initiate these events remain poorly understood. The inventors identify the nuclear alarmin interleukin (IL)-33 as an initiation factor of tissue injury and also as a major amplification factor of the innate immune response triggered by experimental kidney ischemia-reperfusion in mice. In mice lacking IL-33, IRI is reduced, as attested by early decreased tubular cell injury, and by subsequent decreased infiltration of IFN-γ / IL-17A-producing neutrophils and preservation of renal functions. These findings led the inventors to propose that endogenous IFN-33 contributes to kidney IRI by promoting iNKT cell recruitment and cytokine production, resulting in neutrophil infiltration and activation at the injury site. Accordingly, the present invention relates to antagonists of IL-33 for use in methods for preventing ischemia reperfusion injury in an organ.

The present invention provides a method of preventing, reducing or attenuating acute kidney injury in a subject at risk of experiencing a transient increase in kidney ischemia or hypoxia, comprising administering to the subject an effective amount of an agent that binds to and neutralizes endogenous ouabain (EO).

The invention relates to the technical field of biomedicine, in particular to tetranectin-mimicking peptide TNP and its application in treating diseases caused by the release of HMGB1 from vascular endothelial cells. The sequence of the acetylated tetranectin mimetic peptide at the nitrogen end is Ac‑QPDGGKTENCAVLSGAANGKWFDKRCRDK‑biotin. The acetylated tetranectin mimetic peptide TNP can effectively prevent the hydrolysis of TNP and prolong its half-life to improve the biological efficacy of the drug. TNP is in use When preparing drugs for the treatment of sepsis and other diseases, it can effectively inhibit the release of HMGB1 from vascular endothelial cells, reduce the concentration of extracellular HMGB1, and reduce the death rate of septic mice, and can almost completely block renal ischemia-reperfusion in mice. Changes in plasma urea nitrogen and creatinine can reduce renal tubular necrosis after ischemia, achieve the purpose of treating acute kidney injury, and provide a new way for the diagnosis and treatment of human diseases caused by the release of HMGB1 from vascular endothelial cells.

An application of Ponatinib as a drug for acute kidney injury. Since PDCD4 aggravates the kidney injury by regulating an Fgr-Stat3-Notch1 pathway, the ponatinib, an Fgr kinase inhibitor, is adopted to treat the acute kidney injury. The drug has a significant protective effect on the injury caused by kidney ischemia reperfusion, and it is indicated that the drug intervention in Fgr can prevent and treat the acute kidney injury.

The invention relates to the field of medicine, in particular to medicine application of a beta subunit of truncated type sodium-potassium atpase. The medicine application of the beta subunit of the truncated type sodium-potassium atpase on the protection effect of ischemia reperfusion injury of islet transplantation is achieved. Protection of tNKA beta on islet cell ischemia reperfusion injury is cleared, and the measure for preventing kidney ischemia reperfusion injury is further optimized. The mechanism of the tNKA beta on the protection effect on the islet cell ischemia reperfusion injury is disclosed, and a theoretical basis is provided for clinical experiments and research. The medicine application of a beta subunit of the truncated type sodium-potassium atpase has the advantages that the situation of inanition can be effectively relieved in the pancreatic islet ischemia reperfusion effect, and the anoxic situation is relieved.