rdf:type |
|
lifeskim:mentions |
umls-concept:C0007634,
umls-concept:C0010453,
umls-concept:C0017262,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0031715,
umls-concept:C0035143,
umls-concept:C0042878,
umls-concept:C0079189,
umls-concept:C0185117,
umls-concept:C0333348,
umls-concept:C0521447,
umls-concept:C1150571,
umls-concept:C1521761,
umls-concept:C1879547,
umls-concept:C2911684
|
pubmed:issue |
11
|
pubmed:dateCreated |
2010-10-25
|
pubmed:abstractText |
Vitamin K is essential for blood coagulation and bone metabolism in mammals. This vitamin functions as a cofactor in the posttranslational synthesis of ?-carboxyglutamic acid (Gla) from glutamic acid residues. However, other functions of vitamin K have been reported recently. We previously found that vitamin K suppresses the inflammatory reaction induced by lipopolysaccharide (LPS) in rats and human macrophage-like THP-1 cells. In this study, we further investigated the mechanism underlying the anti-inflammatory effect of vitamin K by using cultures of LPS-treated human- and mouse-derived cells. All the vitamin K analogues analyzed in our study exhibited varied levels of anti-inflammatory activity. The isoprenyl side chain structures, except geranylgeraniol, of these analogues did not show such activity; warfarin did not interfere with this activity. The results of our study suggest that the 2-methyl-1,4-naphtoquinone ring structure contributes to express the anti-inflammatory activity, which is independent of the Gla formation activity of vitamin K. Furthermore, menaquinone-4, a form of vitamin K?, reduced the activation of nuclear factor ?B (NF?B) and inhibited the phosphorylation of IKK?/? after treatment of cells with LPS. These results clearly show that the anti-inflammatory activity of vitamin K is mediated via the inactivation of the NF?B signaling pathway.
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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/1-Carboxyglutamic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Inflammatory Agents,
http://linkedlifedata.com/resource/pubmed/chemical/CHUK protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Chuk protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/I-kappa B Kinase,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Vitamin K
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
|
pubmed:issn |
1873-4847
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pubmed:author |
|
pubmed:copyrightInfo |
Copyright © 2010 Elsevier Inc. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:volume |
21
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1120-6
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pubmed:meshHeading |
pubmed-meshheading:20149620-1-Carboxyglutamic Acid,
pubmed-meshheading:20149620-Animals,
pubmed-meshheading:20149620-Anti-Inflammatory Agents,
pubmed-meshheading:20149620-Blotting, Western,
pubmed-meshheading:20149620-Cell Line,
pubmed-meshheading:20149620-Cytokines,
pubmed-meshheading:20149620-Humans,
pubmed-meshheading:20149620-I-kappa B Kinase,
pubmed-meshheading:20149620-Interleukin-6,
pubmed-meshheading:20149620-Lipopolysaccharides,
pubmed-meshheading:20149620-Mice,
pubmed-meshheading:20149620-Mice, Inbred C57BL,
pubmed-meshheading:20149620-NF-kappa B,
pubmed-meshheading:20149620-Phosphorylation,
pubmed-meshheading:20149620-RNA, Messenger,
pubmed-meshheading:20149620-Vitamin K
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pubmed:year |
2010
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pubmed:articleTitle |
Vitamin K suppresses the lipopolysaccharide-induced expression of inflammatory cytokines in cultured macrophage-like cells via the inhibition of the activation of nuclear factor ?B through the repression of IKK?/? phosphorylation.
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pubmed:affiliation |
Laboratory of Nutrition, Graduate School of Agricultural Science, Tohoku University, Sendai 981-8555, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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