Linked Life Data

14713338

Source:http://linkedlifedata.com/resource/pubmed/id/14713338

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2004-1-9
pubmed:abstractText
Thioredoxin (TRX) is induced by a variety of oxidative stimuli and shows cytoprotective roles against oxidative stress. To clarify the possibility of clinical application, we examined the effects of intravenously administered TRX in a model of transient focal cerebral ischemia in this study. Mature male C57BL/6j mice received either continuous intravenous infusion of recombinant human TRX (rhTRX) over a range of 1-10 mg/kg, bovine serum albumin, or vehicle alone for 2 h after 90-min transient middle cerebral artery occlusion (MCAO). Twenty-four hours after the transient MCAO, the animals were evaluated neurologically and the infarct volumes were assessed. Infarct volume, neurological deficit, and protein carbonyl contents, a marker of protein oxidation, in the brain were significantly ameliorated in rhTRX-treated mice at the dose of 3 and 10 mg/kg versus these parameters in control animals. Moreover, activation of p38 mitogen-activated protein kinase, whose pathway is involved in ischemic neuronal death, was suppressed in the rhTRX-treated mice. Further, rhTRX was detected in the ischemic hemisphere by western blot analysis, suggesting that rhTRX was able to permeate the blood-brain barrier in the ischemic hemisphere. These data indicate that exogenous TRX exerts distinct cytoprotective effects on cerebral ischemia/reperfusion injury in mice by means of its redox-regulating activity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1523-0864
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
81-7
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:14713338-Animals, pubmed-meshheading:14713338-Brain, pubmed-meshheading:14713338-Brain Infarction, pubmed-meshheading:14713338-Disease Models, Animal, pubmed-meshheading:14713338-Dose-Response Relationship, Drug, pubmed-meshheading:14713338-Humans, pubmed-meshheading:14713338-Injections, Intravenous, pubmed-meshheading:14713338-Ischemic Attack, Transient, pubmed-meshheading:14713338-Male, pubmed-meshheading:14713338-Mice, pubmed-meshheading:14713338-Mice, Inbred C57BL, pubmed-meshheading:14713338-Mitogen-Activated Protein Kinases, pubmed-meshheading:14713338-Oxidation-Reduction, pubmed-meshheading:14713338-Proteins, pubmed-meshheading:14713338-Recombinant Proteins, pubmed-meshheading:14713338-Thioredoxins, pubmed-meshheading:14713338-p38 Mitogen-Activated Protein Kinases
pubmed:year
2004
pubmed:articleTitle
Intravenous administration of thioredoxin decreases brain damage following transient focal cerebral ischemia in mice.
pubmed:publicationType
Letter, Research Support, Non-U.S. Gov't