Source:http://linkedlifedata.com/resource/pubmed/id/14597987
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
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| pubmed:dateCreated |
2003-11-4
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| pubmed:abstractText |
The regulated expression of adhesion molecules on the surface of endothelial cells is a key process in the pathogenesis of inflammation. The saponin astragaloside IV (AS-IV), a 3-O-beta-D-xylopyranosyl-6-O-beta-D-glucopyranosylcycloastragenol purified from the Chinese medical herb Astragalus membranaceus (Fisch) Bge. has been shown to have anti-inflammatory effects in vivo. In this study we have investigated the effect of AS-IV on cytokine-and LPS-stimulated expression of adhesion molecules in and leukocyte adhesion to endothelial cells. We have demonstrated that AS-IV significantly reduced the adhesion promoting activity of LPS-stimulated HUVECs for polymorph-nuclear leukocytes (PMNs) and the monocytic cell line THP-1. Furthermore, by using specific cell ELISAs we could show that AS-IV decreased the LPS-induced expression of E-selectin and VCAM-1 on the surface of HUVECs in a dose and time dependent manner, whereas the expression of ICAM-1 was not affected by AS-IV. AS-IV also inhibits TNFalpha-induced VCAM-1 expression. The saponin octyl-D-glucopyranoside had no effect on the LPS-induced expression of E-selectin and VCAM-1 excluding an unspecific detergent-like effect of AS-IV. Moreover, AS-IV significantly inhibited LPS- and TNFalpha-induced specific mRNA levels for E-selectin and VCAM-1. Finally, we could show that AS-IV completely abolished LPS- and TNFalpha-induced nuclear translocation of NF-kappaB and NF-kappaB DNA binding activity in endothelial cells. We conclude that the ability of AS-IV to inhibit the NF-kappaB pathway might be one under-lying mechanism contributing to its anti-inflammatory potential in vivo.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Inflammatory Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Cell Adhesion Molecules,
http://linkedlifedata.com/resource/pubmed/chemical/Drugs, Chinese Herbal,
http://linkedlifedata.com/resource/pubmed/chemical/E-Selectin,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Adhesion Molecule-1,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Saponins,
http://linkedlifedata.com/resource/pubmed/chemical/Triterpenes,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Cell Adhesion Molecule-1,
http://linkedlifedata.com/resource/pubmed/chemical/astragaloside A
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| pubmed:status |
MEDLINE
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| pubmed:month |
Nov
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| pubmed:issn |
0340-6245
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
90
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
904-14
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:14597987-Anti-Inflammatory Agents,
pubmed-meshheading:14597987-Cell Adhesion,
pubmed-meshheading:14597987-Cell Adhesion Molecules,
pubmed-meshheading:14597987-Cells, Cultured,
pubmed-meshheading:14597987-Drugs, Chinese Herbal,
pubmed-meshheading:14597987-E-Selectin,
pubmed-meshheading:14597987-Endothelium, Vascular,
pubmed-meshheading:14597987-Humans,
pubmed-meshheading:14597987-Intercellular Adhesion Molecule-1,
pubmed-meshheading:14597987-Leukocytes,
pubmed-meshheading:14597987-Lipopolysaccharides,
pubmed-meshheading:14597987-NF-kappa B,
pubmed-meshheading:14597987-Saponins,
pubmed-meshheading:14597987-Triterpenes,
pubmed-meshheading:14597987-Tumor Necrosis Factor-alpha,
pubmed-meshheading:14597987-Umbilical Veins,
pubmed-meshheading:14597987-Vascular Cell Adhesion Molecule-1
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| pubmed:year |
2003
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| pubmed:articleTitle |
Antiinflammatory activity of astragaloside IV is mediated by inhibition of NF-kappaB activation and adhesion molecule expression.
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| pubmed:affiliation |
Department of Vascular Biology and Thrombosis Research, University of Vienna, Austria.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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