Linked Life Data

14625480

Source:http://linkedlifedata.com/resource/pubmed/id/14625480

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2003-11-19
pubmed:abstractText
The salutary effects of high-density lipoproteins (HDLs) in animal and human models of endotoxic shock have in the past been attributed to the ability of this lipoprotein to bind to lipopolysaccharide. However, the precise mechanisms for the protective effect of HDL are unclear. The first objective of this study was to determine the effects of HDLs on the organ injury and dysfunction associated with acute severe endotoxemia. Second, to gain insight into the mechanism of action of HDL, we also investigated the effect of HDLs on 1) the expression of P-selectin and intercellular adhesion molecule-1 in the kidneys of rats treated with endotoxin and 2) the rise in the plasma levels of tumor necrosis factor-alpha (TNF-alpha). Rats were given Escherichia coli lipopolysaccharide (6 mg/kg i.v.), pretreated with either vehicle (n = 9) or reconstituted HDL (rHDL; apolipoprotein A-I/phosphatidylcholine proteoliposomes, n = 10), and were monitored for 6 h. Here we report that rHDL attenuates the renal injury and dysfunction caused by endotoxin in the rat. In addition, rHDL reduced the degree of histological tissue injury in the lung, liver and intestine and attenuated the expression of P-selectin and intercellular adhesion molecule-1 in the renal glomerulus. Interestingly, pretreatment of rats with rHDL did not prevent the hypotension nor the rise in plasma levels of TNF-alpha (at 90 min) caused by endotoxin. Thus, rHDL reduces the organ injury/dysfunction, but does not affect the circulatory failure, nor the rise in plasma levels of TNF-alpha caused by endotoxin in the rat. We propose that the mechanisms of these beneficial effects of HDL may be related to direct inhibition of adhesion molecule expression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1073-2322
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
551-7
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:14625480-Alanine Transaminase, pubmed-meshheading:14625480-Animals, pubmed-meshheading:14625480-Aspartate Aminotransferases, pubmed-meshheading:14625480-Endotoxemia, pubmed-meshheading:14625480-Endotoxins, pubmed-meshheading:14625480-Escherichia coli, pubmed-meshheading:14625480-Immunohistochemistry, pubmed-meshheading:14625480-Intercellular Adhesion Molecule-1, pubmed-meshheading:14625480-Intestine, Small, pubmed-meshheading:14625480-Kidney, pubmed-meshheading:14625480-Lipase, pubmed-meshheading:14625480-Lipopolysaccharides, pubmed-meshheading:14625480-Lipoproteins, HDL, pubmed-meshheading:14625480-Liver, pubmed-meshheading:14625480-Lung Injury, pubmed-meshheading:14625480-Male, pubmed-meshheading:14625480-P-Selectin, pubmed-meshheading:14625480-Rats, pubmed-meshheading:14625480-Rats, Wistar, pubmed-meshheading:14625480-Shock, pubmed-meshheading:14625480-Shock, Septic, pubmed-meshheading:14625480-Time Factors, pubmed-meshheading:14625480-Tumor Necrosis Factor-alpha
pubmed:year
2003
pubmed:articleTitle
Reconstituted high-density lipoprotein attenuates organ injury and adhesion molecule expression in a rodent model of endotoxic shock.
pubmed:affiliation
Department of Experimental Medicine Nephrology & Critical Care, The William Harvey Research Institute, St. Bartholomew's and The Royal London School of Medicine and Dentistry, Queen Mary, University of London, Charterhouse Square, London, United Kingdom.
pubmed:publicationType
Journal Article