Linked Life Data

10501189

Source:http://linkedlifedata.com/resource/pubmed/id/10501189

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1999-10-14
pubmed:abstractText
In recent years inflammatory mechanisms have become increasingly appreciated as important steps in the Alzheimer's pathogenic pathway. There is accumulating evidence that amyloid beta-peptide (A beta), the peptide product of the cleavage of amyloid precursor protein, may promote or exacerbate local inflammation by stimulating glial cells to release immune mediators. In addition, clinical studies using nonsteroidal antiinflammatory drugs have found a reduced risk for Alzheimer's disease with their use. Here we show that the neurotoxic A beta, a major plaque component, and lipopolysaccharides (LPS), an immune reaction-triggering portion of bacterial membranes, are both potent activators of the nuclear transcription factor NF-kappaB in primary rat astroglial cells. The activation was found to be concentration- and time-dependent and could be attenuated in the presence of NF-kappaB decoy nucleotides. The pretreatment by either 17beta-estradiol (1-10 microg) or sodium salicylate (3-30 mM) reduced the A beta (LPS)-induced activation of NF-kappaB by 48 (50%) and 60% (50%) of activated levels, respectively. In addition, 17beta-estradiol (10 microM) and sodium salicylate (10 mM) were able to attenuate the increase in interleukin-1beta levels following exposure to 25 microM A beta. Our data suggest that the aberrant gene expression is at least in part due to A beta-induced activation of NF-kappaB, a potent immediate-early transcriptional regulator of numerous proinflammatory genes; this event takes place in astroglial cells. The results of our experiments provide a further understanding of the effects of estrogen and aspirin on astroglial cells exposed to A beta and LPS.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
73
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1453-60
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Sodium salicylate and 17beta-estradiol attenuate nuclear transcription factor NF-kappaB translocation in cultured rat astroglial cultures following exposure to amyloid A beta(1-40) and lipopolysaccharides.
pubmed:affiliation
Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis 46202, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't