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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5-6
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pubmed:dateCreated |
2002-7-29
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pubmed:abstractText |
Flavonoids are natural polyphenolic compounds ubiquitously present in the plant kingdom. They are reported to exhibit numerous beneficial health effects. In the present study, we demonstrate the potential effects of different flavonoids on cytokines mediated cyclooxygenase-2 and inducible nitric oxide synthase expression and activities in A549 cell line using quercetin, amentoflavone and flavanone. Our data revealed that quercetin, at 50 micro M concentration inhibited PGE(2) biosynthesis by A549 very strongly with little effect on COX-2 mRNA and protein expression. Unlike quercetin, amentoflavone inhibited both PGE(2) biosynthesis and COX-2 mRNA and protein expression strongly. In another set of experiment, quercetin inhibited iNOS protein expression completely without affecting iNOS mRNA expression. In contrast, amentoflavone although exerted no inhibitory effect on iNOS mRNA expression, did inhibit weakly iNOS protein expression. Flavanone had no inhibitory effect on either enzyme at the same concentration. Taken together, our data indicated that amentoflavone and quercetin differentially exerted supression of PGE(2) biosynthesis via downregulation of COX-2/iNOS expression.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Biflavonoids,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase 2,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone,
http://linkedlifedata.com/resource/pubmed/chemical/Flavonoids,
http://linkedlifedata.com/resource/pubmed/chemical/Isoenzymes,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/NOS2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II,
http://linkedlifedata.com/resource/pubmed/chemical/PTGS2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Prostaglandin-Endoperoxide Synthases,
http://linkedlifedata.com/resource/pubmed/chemical/Quercetin,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/amentoflavone
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pubmed:status |
MEDLINE
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pubmed:issn |
0952-3278
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
66
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
485-92
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pubmed:dateRevised |
2011-10-27
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pubmed:meshHeading |
pubmed-meshheading:12144868-Adenocarcinoma,
pubmed-meshheading:12144868-Biflavonoids,
pubmed-meshheading:12144868-Blotting, Western,
pubmed-meshheading:12144868-Cyclooxygenase 2,
pubmed-meshheading:12144868-Cytokines,
pubmed-meshheading:12144868-Dinoprostone,
pubmed-meshheading:12144868-Dose-Response Relationship, Drug,
pubmed-meshheading:12144868-Down-Regulation,
pubmed-meshheading:12144868-Enzyme Induction,
pubmed-meshheading:12144868-Flavonoids,
pubmed-meshheading:12144868-Humans,
pubmed-meshheading:12144868-Immunoassay,
pubmed-meshheading:12144868-Isoenzymes,
pubmed-meshheading:12144868-Lung Neoplasms,
pubmed-meshheading:12144868-Membrane Proteins,
pubmed-meshheading:12144868-Nitric Oxide,
pubmed-meshheading:12144868-Nitric Oxide Synthase,
pubmed-meshheading:12144868-Nitric Oxide Synthase Type II,
pubmed-meshheading:12144868-Prostaglandin-Endoperoxide Synthases,
pubmed-meshheading:12144868-Quercetin,
pubmed-meshheading:12144868-RNA, Messenger,
pubmed-meshheading:12144868-Tumor Cells, Cultured
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pubmed:articleTitle |
Downregulation of COX-2 and iNOS by amentoflavone and quercetin in A549 human lung adenocarcinoma cell line.
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pubmed:affiliation |
Center For Comparative Lung Cell Biology and Medicine, School of Medicine, Division of Pulmonary Critical Care Medicine, University of California, Davis, CA 95616, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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