Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
1996-12-20
|
| pubmed:abstractText |
During the past several years, it has become increasingly apparent that interleukin-1 (IL-1), particularly IL-1 beta plays an important role in brain injury during ischemia. Studies from various laboratories have shown that IL-1 beta mRNA and IL-1 beta protein are synthesized early in ischemia and that the injection of IL-1 beta into ischemic brain enhances edema formation. The most direct evidence that IL-1 beta contributes to ischemic injury, however, is the demonstration that infarct volume in focal ischemia is reduced following intraventricular injection of an endogenous interleukin-1 receptor antagonist (IL-1ra), or after IL-1ra is overexpressed in brain using an adenoviral vector to transfer IL-1ra cDNA to brain cells. Ischemic injury is also reduced in mice that fail to produce IL-1 beta because of an abnormal interleukin-1 beta converting enzyme gene (ICE knockout mice). At the present time, it is nuclear how IL-1 beta causes brain injury, but several possible mechanisms include 1) stimulation of an inflammatory response through the activation of glia or the induction of other cytokines and/or endothelial adhesion molecules and 2) release of free radicals through stimulation of arachidonic acid metabolism and/or nitric oxide synthase activity.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Sep
|
| pubmed:issn |
0022-9717
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
45
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
230-7; discussion 238
|
| pubmed:dateRevised |
2008-8-7
|
| pubmed:meshHeading | |
| pubmed:year |
1996
|
| pubmed:articleTitle |
Interleukin-1 in cerebral ischemia.
|
| pubmed:affiliation |
Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor 48109-0532, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|