Document Detail


Acetylbritannilatone suppresses NO and PGE2 synthesis in RAW 264.7 macrophages through the inhibition of iNOS and COX-2 gene expression.
MedLine Citation:
PMID:  15172177     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In order to elucidate the mechanism of anti-inflammatory effect of 1-o-acetylbritannilatone (ABL) isolated from Inula Britannica-F, we investigated ABL for its ability to inhibit the inflammatory factor production in RAW 264.7 macrophages. The studies showed that ABL not only inhibited LPS/IFN-gamma-mediated nitric oxide (NO) production and inducible nitric synthase (iNOS) expression, but also decreased LPS/IFN-gamma-induced prostaglandin E2 (PGE2) production and cyclo-oxygenase-2 (COX-2) expression in a concentration-dependent manner. EMSA demonstrated that ABL inhibited effectively the association of NF-kappaB, which is necessary for the expression of iNOS and COX-2, with its binding motif in the promoter of target genes. These data suggest that ABL suppress NO and PGE2 synthesis in RAW 264.7 macrophages through the inhibition of iNOS and COX-2 gene expression, respectively. The anti-inflammatory effect of ABL involves blocking the binding of NF-kappaB to the promoter in the target genes and inhibiting the expression of iNOS and COX-2.
Authors:
Mei Han; Jin-Kun Wen; Bin Zheng; Di-Qun Zhang
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Life sciences     Volume:  75     ISSN:  0024-3205     ISO Abbreviation:  Life Sci.     Publication Date:  2004 Jun 
Date Detail:
Created Date:  2004-06-02     Completed Date:  2004-07-15     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0375521     Medline TA:  Life Sci     Country:  England    
Other Details:
Languages:  eng     Pagination:  675-84     Citation Subset:  IM    
Copyright Information:
Copyright 2004 Elsevier Inc.
Affiliation:
Department of Biochemistry and Molecular Biology, Institute of Basic Medicine, Hebei Medical University, No. 361, Zhongshan East Road, Shijiazhuang, 050017, PR China.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anti-Inflammatory Agents / pharmacology*
Cell Line
Cyclooxygenase 2
Dinoprostone / biosynthesis*
Dose-Response Relationship, Drug
Drug Combinations
Gene Expression Regulation, Enzymologic / drug effects*
Interferon-gamma / pharmacology
Isoenzymes / biosynthesis,  genetics*
Lactones / pharmacology*
Lipopolysaccharides / pharmacology
Macrophages / drug effects*,  enzymology
Mice
NF-kappa B / metabolism
Nitric Oxide / biosynthesis*
Nitric Oxide Synthase / biosynthesis,  genetics*
Nitric Oxide Synthase Type II
Prostaglandin-Endoperoxide Synthases / biosynthesis,  genetics*
RNA, Messenger / genetics,  metabolism
Reverse Transcriptase Polymerase Chain Reaction
Chemical
Reg. No./Substance:
0/Anti-Inflammatory Agents; 0/Drug Combinations; 0/Isoenzymes; 0/Lactones; 0/Lipopolysaccharides; 0/NF-kappa B; 0/RNA, Messenger; 0/acetylbritannilatone; 10102-43-9/Nitric Oxide; 363-24-6/Dinoprostone; 82115-62-6/Interferon-gamma; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.13.39/Nos2 protein, mouse; EC 1.14.99.1/Cyclooxygenase 2; EC 1.14.99.1/Prostaglandin-Endoperoxide Synthases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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