http://rdf.ncbi.nlm.nih.gov/pubchem/patent/EP-3046570-A1

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classificationIPCInventive http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K38-00
filingDate 2014-09-22-04:00^^<http://www.w3.org/2001/XMLSchema#date>
inventor http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_5e7c436191fc34aa493a31427d25df4b
publicationDate 2016-07-27-04:00^^<http://www.w3.org/2001/XMLSchema#date>
publicationNumber EP-3046570-A1
titleOfInvention Compositions and methods for protecting the kidney from ischemia reperfusion injury
abstract The effects of hepcidin treatment on mitigating IRI and acute kidney injury by decreasing iron availability and ROS-mediated cell death were tested. C57Bl/6 (WT) and hepcidin knock out (Hamp -/-) mice were treated with saline or 50 μg of hepcidin i.p. prior to bilateral renal IRI. Renal function, injury markers, histopathology, and inflammation were examined after 24 hours of reperfusion. In WT mice, IRI induced increases in serum and kidney non-heme iron levels, but hepcidin treatment induced sequestration of iron in the spleen and liver and prevented IRI-associated increases in serum and kidney non-heme iron. Kidney function was significantly better in hepcidin-treated mice, accompanied by less acute tubular necrosis and reduced infiltration of immune cells. Hepcidin treatment decreased kidney ferroportin expression and induced the expression of cytoprotectant, H-Ferritin, and was associated with less ROS and tubular epithelial apoptosis. These results demonstrate a protective role of hepcidin in IRI and AKI.
priorityDate 2013-09-20-04:00^^<http://www.w3.org/2001/XMLSchema#date>
type http://data.epo.org/linked-data/def/patent/Publication

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