Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2002-10-24
pubmed:abstractText
The mechanisms by which nitric oxide (NO) exerts its protective effect in the ischemia/reperfusion (I/R) injury of the kidney have not been fully determined. The hypothesis of this study was based on the assumption that I/R upregulates some chemokines (MIP-2 and MIP-1alpha) as well as certain protein kinases (MAPK p44/42), and therefore we aimed in this work at recognizing if an exogenous NO donor would downregulate these effects in rat ischemic kidneys at the same time that it would offer functional protection as measured by serum creatinine. Sprague-Dawley rats were subjected to renal warm ischemia (75 min) and contralateral nephrectomy. Animals were divided into 3 groups (n = 8 per group): sham, ischemic control, and ischemic group treated with sodium nitroprusside (NaNP 5 mg/kg) given 15 min prior to reperfusion. Serum creatinine (SCr), serum chemokines (MIP-2 and MIP-1alpha), kidney tissue MAPK p44/42, kidney neutrophil infiltration determined by myeloperoxidase (MPO), and light histology were evaluated 4 h after reperfusion began. There were significant improvements in SCr and better histopathological features in the I/R-NaNP group compared with the I/R group. Similarly, the I/R-NaNP kidneys exhibited a downregulating effect of serum chemokines (MIP-2 and MIP-1alpha) and kidney tissue MAPK p44/42 that was not observed in the I/R group alone. The MPO levels were lower in the I/R-NaNP group compared with the I/R untreated group. We can conclude from these experiments that I/R of the rat kidney upregulated the production of MIP-2 and MIP-1alpha chemokines and the activation of MAPKp44/42. It also had a detrimental effect on the function and structure of the ischemic kidney. Exogenous NO had a temporal protective effect in organ function and histology and exerted a downregulating response in the production of MIP-2 and MIP-1alpha chemokines and the activation of MAPK p44/42 following I/R.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL3, http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL4, http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL2, http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CXC, http://linkedlifedata.com/resource/pubmed/chemical/Cxcl2 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Signaling Peptides..., http://linkedlifedata.com/resource/pubmed/chemical/Macrophage Inflammatory Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 1, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 3, http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Monokines, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Donors, http://linkedlifedata.com/resource/pubmed/chemical/Nitroprusside
pubmed:status
MEDLINE
pubmed:issn
0894-1939
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
287-96
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:12396433-Animals, pubmed-meshheading:12396433-Chemokine CCL3, pubmed-meshheading:12396433-Chemokine CCL4, pubmed-meshheading:12396433-Chemokine CXCL2, pubmed-meshheading:12396433-Chemokines, CXC, pubmed-meshheading:12396433-Down-Regulation, pubmed-meshheading:12396433-Intercellular Signaling Peptides and Proteins, pubmed-meshheading:12396433-Kidney, pubmed-meshheading:12396433-MAP Kinase Signaling System, pubmed-meshheading:12396433-Macrophage Inflammatory Proteins, pubmed-meshheading:12396433-Male, pubmed-meshheading:12396433-Mitogen-Activated Protein Kinase 1, pubmed-meshheading:12396433-Mitogen-Activated Protein Kinase 3, pubmed-meshheading:12396433-Mitogen-Activated Protein Kinases, pubmed-meshheading:12396433-Monokines, pubmed-meshheading:12396433-Nitric Oxide, pubmed-meshheading:12396433-Nitric Oxide Donors, pubmed-meshheading:12396433-Nitroprusside, pubmed-meshheading:12396433-Rats, pubmed-meshheading:12396433-Rats, Sprague-Dawley, pubmed-meshheading:12396433-Reperfusion Injury
pubmed:articleTitle
Exogenous nitric oxide downregulates MIP-2 and MIP-1alpha chemokines and MAPK p44/42 after ischemia and reperfusion of the rat kidney.
pubmed:affiliation
Department of Surgery Research Sciences, Trauma and Molecular Biology, Borgess Research Institute, Kalamazoo, Michigan 49001, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't