rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
1999-1-29
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pubmed:abstractText |
The induction of the inducible nitric oxide synthase (iNOS) has been proposed to play a role in a variety of inflammatory diseases. Sodium salicylate (NaSal) is the most commonly used anti-inflammatory agent. We investigated whether NaSal can diminish the induction of iNOS in murine brain microglial cells. In primary cultures, interferon-gamma (IFN-gamma) or lipopolysaccharide (LPS) separately did not stimulate nitric oxide (NO) production, whereas IFN-gamma combined with LPS synergistically induced iNOS. NaSal inhibited both the production of NO and expression of iNOS in microglial cells. Synergy between IFN-gamma and LPS was mainly dependent on tumour necrosis factor-alpha (TNF-alpha) secretion as the increase of the induction of the iNOS by IFN-gamma plus LPS was associated with the increase of TNF-alpha secretion and IFN-gamma plus LPS-induced TNF-alpha secretion by microglial cells was decreased by the treatment with NaSal. These results suggest a possible use of NaSal in managing inflammation of the central nervous system through inhibition of the iNOS induction.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-1373522,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-1383325,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-2056249,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-2111344,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-2115549,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-2636710,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-2878227,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-3491140,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-3494200,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-3495737,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-3543052,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-5432063,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-6982921,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-7508926,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-7510883,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-7517676,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-7522969,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-7522970,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-7530002,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-7535524,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-7544010,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-7671126,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-7684434,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-7692452,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-7759887,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-7920028,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-7923361,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-8052854,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-8135804,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-8170969,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-8300158,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9824502-8910280
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0019-2805
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:volume |
95
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
389-94
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:9824502-Animals,
pubmed-meshheading:9824502-Anti-Inflammatory Agents, Non-Steroidal,
pubmed-meshheading:9824502-Brain,
pubmed-meshheading:9824502-Cell Culture Techniques,
pubmed-meshheading:9824502-Cyclooxygenase Inhibitors,
pubmed-meshheading:9824502-Drug Synergism,
pubmed-meshheading:9824502-Interferon-gamma,
pubmed-meshheading:9824502-Lipopolysaccharides,
pubmed-meshheading:9824502-Mice,
pubmed-meshheading:9824502-Mice, Inbred BALB C,
pubmed-meshheading:9824502-Microglia,
pubmed-meshheading:9824502-Nitric Oxide,
pubmed-meshheading:9824502-Nitric Oxide Synthase,
pubmed-meshheading:9824502-Recombinant Proteins,
pubmed-meshheading:9824502-Sodium Salicylate,
pubmed-meshheading:9824502-Tumor Necrosis Factor-alpha
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pubmed:year |
1998
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pubmed:articleTitle |
Inhibition of the induction of the inducible nitric oxide synthase in murine brain microglial cells by sodium salicylate.
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pubmed:affiliation |
College of Pharmacy, Wonkwang University, Iksan, Chonbuk, 570-749, South Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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