Linked Life Data

9110410

Source:http://linkedlifedata.com/resource/pubmed/id/9110410

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1997-6-19
pubmed:abstractText
A prospective, randomized model of LD100/24 h endotoxemia was performed in male Wistar rats (n = 26; 250-300 g). The animals were divided into four groups: Group I (n = 5; saline treatment only), Group II (n = 5; Zn2+ treatment only), Group III (n = 8; saline pretreatment, lipopolysaccharide (LPS) treatment), and Group IV (n = 8; Zn2+ pretreatment, LPS treatment). Zn2+ pretreatment was carried out by intraperitoneal injection of 50 mg/kg zinc-bis-(DL-hydrogenaspartate) (10 mg/kg Zn2+). LD100/24 h endotoxemia was induced by intraperitoneal administration of 20 mg/kg LPS of the Escherichia coli strain WO111:B4. Tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 were detected by enzyme-linked immunosorbent assay (ELISA). HSP70 expression in the lungs, the liver, and the kidneys was determined by immunohistochemistry, Western blotting, and an HSP70 ELISA. Apoptosis was also detected by an in situ apoptosis detection kit (TUNEL) and a cell death detection ELISA, respectively. This rat model of endotoxemia proves the close relationship between HSP70 expression, cytokine liberation, and development of apoptosis. The data demonstrate that: 1) Zn2+ is a potent inducer of HSP70 expression; 2) the application of Zn2+ leads to slightly increased cytokine plasma levels; and 3) the manipulation of the heat shock response by Zn2+ significantly increases the survival rate after LD100 endotoxemia. Enhanced survival rate in animals pretreated with Zn2+ may be explained by increased tissue levels of HSP70, a subsequent significantly decreased liberation of the proinflammatory cytokines after LPS challenge, and a significantly decreased rate of apoptosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1073-2322
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
254-62
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:9110410-Animals, pubmed-meshheading:9110410-Apoptosis, pubmed-meshheading:9110410-Aspartic Acid, pubmed-meshheading:9110410-Blotting, Western, pubmed-meshheading:9110410-Cytokines, pubmed-meshheading:9110410-Disease Models, Animal, pubmed-meshheading:9110410-Dose-Response Relationship, Drug, pubmed-meshheading:9110410-Endotoxemia, pubmed-meshheading:9110410-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:9110410-HSP70 Heat-Shock Proteins, pubmed-meshheading:9110410-Immunohistochemistry, pubmed-meshheading:9110410-Interleukin-1, pubmed-meshheading:9110410-Interleukin-6, pubmed-meshheading:9110410-Kidney, pubmed-meshheading:9110410-Lipopolysaccharides, pubmed-meshheading:9110410-Liver, pubmed-meshheading:9110410-Lung, pubmed-meshheading:9110410-Male, pubmed-meshheading:9110410-Microscopy, pubmed-meshheading:9110410-Organometallic Compounds, pubmed-meshheading:9110410-Rats, pubmed-meshheading:9110410-Rats, Wistar, pubmed-meshheading:9110410-Survival Rate, pubmed-meshheading:9110410-Tumor Necrosis Factor-alpha, pubmed-meshheading:9110410-Zinc, pubmed-meshheading:9110410-Zinc Compounds
pubmed:year
1997
pubmed:articleTitle
Induction of heat shock protein 70 by zinc-bis-(DL-hydrogenaspartate) reduces cytokine liberation, apoptosis, and mortality rate in a rat model of LD100 endotoxemia.
pubmed:affiliation
Institute of Pathology, Technical University of Aachen, Germany.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't