Linked Life Data

11238717

Source:http://linkedlifedata.com/resource/pubmed/id/11238717

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2001-3-12
pubmed:abstractText
beta-Amyloid peptides (Abetas) share with lipopolysaccharide, a potent pro-inflammatory agent, the property of stimulating glial cells or macrophages to induce various inflammatory mediators. We recently reported that central administration of lipopolysaccharide induces peripheral interleukin-6 responses via both the central and peripheral norepinephrine system. In this study, the effect of intracerebroventricular injection of various synthetic Abetas on plasma interleukin-6 levels was examined in mice. Abeta(1-42) dose-dependently increased plasma interleukin-6 levels: 'aged' Abeta(1-42) was more effective than fresh, whereas Abeta(42-1) had no effect. 'Aged' Abeta(1-42) (205 pmol/mouse i.c.v.)-induced plasma interleukin-6 peaked at 2 h post injection, which is earlier than the peak time of the Abeta(1-42)-induced brain interleukin-6, tumor necrosis factor-alpha and interleukin-1beta levels, which was 4, 4 and 24 h, respectively. Among various peripheral organs, Abeta(1-42) (205 pmol/mouse i.c.v.) significantly increased interleukin-6 mRNA expression in lymph nodes and liver. Abeta(1-42) (205 pmol/mouse i.c.v.) significantly increased norepinephrine turnover in both hypothalamus and spleen. Either central or peripheral norepinephrine depletion effectively inhibited the Abeta(1-42)-induced peripheral interleukin-6 response. Pretreatment with prazosin (alpha(1)-adrenergic antagonist), yohimbine (alpha(2)-adrenergic antagonist), and ICI-118,551 (beta(2)-adrenergic antagonist), but not with betaxolol (beta(1)-adrenergic antagonist), inhibited Abeta(1-42)-induced plasma interleukin-6 levels. These results demonstrate that centrally administered Abeta(1-42) effectively induces the systemic interleukin-6 response which is mediated, in part, by central Abeta(1-42)-induced activation of the central and the peripheral norepinephrine systems.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
76
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1326-35
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:11238717-Amyloid beta-Peptides, pubmed-meshheading:11238717-Animals, pubmed-meshheading:11238717-Brain, pubmed-meshheading:11238717-Cerebral Ventricles, pubmed-meshheading:11238717-Gene Expression Regulation, pubmed-meshheading:11238717-Injections, Intraventricular, pubmed-meshheading:11238717-Interleukin-1, pubmed-meshheading:11238717-Interleukin-6, pubmed-meshheading:11238717-Kinetics, pubmed-meshheading:11238717-Male, pubmed-meshheading:11238717-Mice, pubmed-meshheading:11238717-Mice, Inbred ICR, pubmed-meshheading:11238717-Norepinephrine, pubmed-meshheading:11238717-Oxidopamine, pubmed-meshheading:11238717-Peptide Fragments, pubmed-meshheading:11238717-RNA, Messenger, pubmed-meshheading:11238717-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:11238717-Structure-Activity Relationship, pubmed-meshheading:11238717-Time Factors, pubmed-meshheading:11238717-Transcription, Genetic, pubmed-meshheading:11238717-Tumor Necrosis Factor-alpha
pubmed:year
2001
pubmed:articleTitle
Central beta-amyloid peptide-induced peripheral interleukin-6 responses in mice.
pubmed:affiliation
Department of Pharmacology, College of Medicine, Institute of Natural Medicine, Hallym University, Chunchon, South Korea. dksong@sun.hallym.ac.kr
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't