Indomethacin corrects alterations associated with ischemia/reperfusion in an in vitro proximal tubular model

American Journal of Nephrology

Volumn 32, Issue 1, 2010, Pages 57-65

  Sauvant, C ^a   Schneider, R ^b   Holzinger, H ^a   Renker, S ^b   Wanner, C ^b   Gekle, M ^c  

^a UNIVERSITY OF WÜRZBURG   (Germany)

^b UNIVERSITY HOSPITAL WÜRZBURG   (Germany)

^c MARTIN LUTHER UNIVERSITY HALLE WITTENBERG   (Germany)

Author keywords

Apoptosis; Dedifferentiation; Fibrosis; Indomethacin; Inducible nitric oxide synthase; Inflammation; Ischemic acute kidney injury; Necrosis; Proximal tubule; Renal ischemia; Reperfusion damage

Indexed keywords

COLLAGEN TYPE 1; COLLAGEN TYPE 3; COLLAGEN TYPE 4; FIBRONECTIN; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; INDOMETACIN; INDUCIBLE NITRIC OXIDE SYNTHASE; MATRIX PROTEIN; MONOCYTE CHEMOTACTIC PROTEIN 1; PROSTAGLANDIN E2; BIOLOGICAL MARKER; CARDIOVASCULAR AGENT; CCL2 PROTEIN, RAT; MESSENGER RNA; NOS2 PROTEIN, RAT; ORGANIC ANION TRANSPORTER;

ANALYTICAL PARAMETERS; ANIMAL CELL; ANIMAL MODEL; ANION TRANSPORT; APOPTOSIS; ARTICLE; BASOLATERAL MEMBRANE; CELL DEATH; CELL LOSS; CELL PROTECTION; CELL SURVIVAL; CLINICAL ASSESSMENT; CONTROLLED STUDY; DRUG EFFECT; EXTRACELLULAR MATRIX; IN VITRO STUDY; INFLAMMATION; INHIBITION KINETICS; KIDNEY CELL CULTURE; KIDNEY ISCHEMIA; KIDNEY PROXIMAL TUBULE; KIDNEY TUBULE CELL; KIDNEY TUBULE NECROSIS; NONHUMAN; PRIORITY JOURNAL; PROSTAGLANDIN RELEASE; PROTEIN INDUCTION; PROTEIN SYNTHESIS; RAT; RENAL PROTECTION; REPERFUSION; TREATMENT OUTCOME; ANIMAL; CELL CULTURE; CYTOLOGY; DRUG EFFECTS; EPITHELIUM CELL; GENETICS; METABOLISM; NECROSIS; OPOSSUM; PATHOLOGY; REPERFUSION INJURY;

ANIMALS; APOPTOSIS; BIOLOGICAL MARKERS; CARDIOVASCULAR AGENTS; CELLS, CULTURED; CHEMOKINE CCL2; DINOPROSTONE; EPITHELIAL CELLS; EXTRACELLULAR MATRIX; IN VITRO TECHNIQUES; INDOMETHACIN; KIDNEY TUBULES, PROXIMAL; NECROSIS; NF-KAPPA B; NITRIC OXIDE SYNTHASE TYPE II; OPOSSUMS; ORGANIC ANION TRANSPORTERS; RATS; REPERFUSION INJURY; RNA, MESSENGER;

EID: 77952986998     PISSN: 02508095     EISSN: None     Source Type: Journal    
DOI: 10.1159/000313452     Document Type: Article

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