Linked Life Data

10899957

Source:http://linkedlifedata.com/resource/pubmed/id/10899957

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-8-17
pubmed:abstractText
Adenosine levels increase in brain during cerebral ischemia, and adenosine has receptor-mediated neuroprotective effects. This study was performed to test the hypothesis that nitrobenzylthioinosine (NBMPR), a selective and potent inhibitor of one adenosine transporter subtype termed ENT1, or es, can protect against ischemic neuronal injury by enhancing adenosine levels and potentiating adenosine receptor-mediated effects, including attenuation of the cellular production and release of tumor necrosis factor-alpha (TNF-alpha). In rats, the phosphorylated prodrug form of NBMPR, NBMPR-phosphate, or saline was administered by intracerebroventricular injection 30 min before forebrain ischemia. Seven days following the ischemic episode, rats were killed, and neuronal damage in the CA1 region of the hippocampus was assessed. The number of pyramidal neurons was significantly (p < 0.001) greater in the NBMPR-P treatment group. A trend toward protection was still evident at 28 days postreperfusion. Adenosine increased significantly during ischemia to levels eight- to 85-fold above basal. NBMPR-P treatment did not cause statistically significant increases in ischemic adenosine levels; however, this treatment tended to increase adenosine levels in all brain regions at 7 min postreperfusion. Ischemia-induced expression of TNF-alpha was not altered by NBMPR-P treatment, and the nonselective adenosine receptor antagonist 8-(p-sulfophenyl) theophylline did not abolish the neuroprotective effects of NBMPR-P treatment. These data indicate that NBMPR can protect CA1 pyramidal neurons from ischemic death without statistically significant effects on adenosine levels or adenosine receptor-mediated inhibition of the proinflammatory cytokine TNF-alpha.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
75
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
795-802
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10899957-Adenosine, pubmed-meshheading:10899957-Affinity Labels, pubmed-meshheading:10899957-Animals, pubmed-meshheading:10899957-Cerebral Ventricles, pubmed-meshheading:10899957-Gene Expression Regulation, pubmed-meshheading:10899957-Injections, Intraventricular, pubmed-meshheading:10899957-Ischemic Attack, Transient, pubmed-meshheading:10899957-Male, pubmed-meshheading:10899957-Neurons, pubmed-meshheading:10899957-Prodrugs, pubmed-meshheading:10899957-Prosencephalon, pubmed-meshheading:10899957-Pyramidal Cells, pubmed-meshheading:10899957-Rats, pubmed-meshheading:10899957-Rats, Sprague-Dawley, pubmed-meshheading:10899957-Receptors, Purinergic P1, pubmed-meshheading:10899957-Reperfusion, pubmed-meshheading:10899957-Thioinosine, pubmed-meshheading:10899957-Thionucleotides, pubmed-meshheading:10899957-Transcription, Genetic, pubmed-meshheading:10899957-Tumor Necrosis Factor-alpha
pubmed:year
2000
pubmed:articleTitle
Effects of nitrobenzylthioinosine on neuronal injury, adenosine levels, and adenosine receptor activity in rat forebrain ischemia.
pubmed:affiliation
Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Canada. fiona_parkinson@umanitoba.ca
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't