Linked Life Data

19060786

Source:http://linkedlifedata.com/resource/pubmed/id/19060786

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-7-16
pubmed:abstractText
Endotoxemia caused by LPS is a life-threatening and inflammatory condition contributing to multiple organ failure. Viruses or bacteria require sialic acid (SA) for target-cell binding. We suggest that exogenous SA through masking or mediating the binding of LPS to the target cells may attenuate LPS-induced liver dysfunction and cecal ligation and puncture-induced shock. We found that SA can directly scavenge O2-, H2O2, and NO activity by a chemiluminescence analyzer and bind to LPS with high affinity using surface plasmon resonance. Intravenous SA significantly increased plasma SA concentration within 4 h. We then assessed the potential effect of SA on LPS-induced acute endotoxemia in the rat. Intravenous LPS (10-50 mg/kg) dose-dependently increased plasma endotoxin and reactive oxygen species in the blood, bile, and liver and increased plasma alanine aminotransferase and aspartate aminotransferase levels as well as TNF-alpha, monocyte chemoattractant protein 1, tissue inhibitor of metalloproteinase 1, IL-1beta, and IL-6 levels in the rats. Thirty minutes after LPS stimulation, SA decreased LPS-enhanced endotoxin level, oxidative stress, alanine aminotransferase and aspartate aminotransferase levels, and cytokine concentration and ameliorated histopathologic alteration in the liver. We found that SA increased LPS-depressed Mn-superoxide dismutase, CuZn-superoxide dismutase, and heat shock protein 70 and decreased LPS-enhanced iNOS and proapoptotic Bax protein expression in the liver by Western blot. Sialic acid was given after treatment to rats subjected to cecal ligation and puncture, and the hypotensive effect was blunted for 6 h. In conclusion, SA treatment can counteract LPS-enhanced acute endotoxemia and oxidative injury via a direct scavenging reactive oxygen species activity and neutralization potential.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1540-0514
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
228-35
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:19060786-Acute Disease, pubmed-meshheading:19060786-Animals, pubmed-meshheading:19060786-Cytokines, pubmed-meshheading:19060786-Drug-Induced Liver Injury, pubmed-meshheading:19060786-Endotoxemia, pubmed-meshheading:19060786-HSP70 Heat-Shock Proteins, pubmed-meshheading:19060786-Hydrogen Peroxide, pubmed-meshheading:19060786-Lipopolysaccharides, pubmed-meshheading:19060786-Liver Diseases, pubmed-meshheading:19060786-Male, pubmed-meshheading:19060786-N-Acetylneuraminic Acid, pubmed-meshheading:19060786-Nitric Oxide, pubmed-meshheading:19060786-Rats, pubmed-meshheading:19060786-Rats, Wistar, pubmed-meshheading:19060786-Superoxide Dismutase, pubmed-meshheading:19060786-Superoxides, pubmed-meshheading:19060786-Time Factors, pubmed-meshheading:19060786-Tissue Inhibitor of Metalloproteinase-1
pubmed:year
2009
pubmed:articleTitle
Sialic acid reduces acute endotoxemia-induced liver dysfunction in the rat.
pubmed:affiliation
Department of Medicine, Kuang-Tien General Hospital, Taichung, Taiwan.
pubmed:publicationType
Journal Article