Resveratrol inhibits Porphyromonas gingivalis lipopolysaccharide-induced endothelial adhesion molecule expression by suppressing NF-kappaB activation

P. gingivalis is a major pathogen that is involved in the onset and progression of periodontal disease. This study investigated the effect of resveratrol, a naturally occurring polyphenol, on P. gingivalis LPS-accelerated vascular inflammation, a key step in the progression of periodontitis. Resvera...

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Veröffentlicht in:Archives of pharmacal research 2009-04, Vol.32 (4), p.583-591
Hauptverfasser: Park, Hyun-Joo, Jeong, Seong-Kyoon, Kim, Su-Ryun, Bae, Soo-Kyung, Kim, Woo-Sik, Jin, Seong-Deok, Koo, Tae Hyeon, Jang, Hye-Ock, Yun, Il, Kim, Kyu-Won, Bae, Moon-Kyoung
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container_issue 4
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container_title Archives of pharmacal research
container_volume 32
creator Park, Hyun-Joo
Jeong, Seong-Kyoon
Kim, Su-Ryun
Bae, Soo-Kyung
Kim, Woo-Sik
Jin, Seong-Deok
Koo, Tae Hyeon
Jang, Hye-Ock
Yun, Il
Kim, Kyu-Won
Bae, Moon-Kyoung
description P. gingivalis is a major pathogen that is involved in the onset and progression of periodontal disease. This study investigated the effect of resveratrol, a naturally occurring polyphenol, on P. gingivalis LPS-accelerated vascular inflammation, a key step in the progression of periodontitis. Resveratrol significantly inhibited the P. gingivalis LPS-induced adhesion of leukocytes to endothelial cells and to the aortic endothelium by down-regulating the cell adhesion molecules, ICAM-1 and VCAM-1. Moreover, the inhibition of the P. gingivalis LPS-induced cell adhesion molecules by resveratrol was mainly mediated by nuclear factor-kappaB (NF-kappaB). Resveratrol suppressed P. gingivalis LPS-stimulated IkappaBalpha phosphorylation and nuclear translocation of the p65 subunit of NF-kappaB in HMECs. Overall, these findings suggest that resveratrol significantly attenuates the P. gingivalis LPS-induced monocyte adhesion to the endothelium by suppressing the expression of the NF-kappaB-dependent cell adhesion molecules, suggesting its therapeutic role in periodontal pathogen-induced vascular inflammation.
doi_str_mv 10.1007/s12272-009-1415-7
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purification</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Male</topic><topic>NF-KappaB Inhibitor alpha</topic><topic>Phosphorylation</topic><topic>Porphyromonas gingivalis - chemistry</topic><topic>Porphyromonas gingivalis - pathogenicity</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>RNA, Messenger - metabolism</topic><topic>Stilbenes - pharmacology</topic><topic>Transcription Factor RelA - metabolism</topic><topic>Transcription, Genetic - drug effects</topic><topic>U937 Cells</topic><topic>Vascular Cell Adhesion Molecule-1 - genetics</topic><topic>Vascular Cell Adhesion Molecule-1 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Park, Hyun-Joo</creatorcontrib><creatorcontrib>Jeong, Seong-Kyoon</creatorcontrib><creatorcontrib>Kim, Su-Ryun</creatorcontrib><creatorcontrib>Bae, Soo-Kyung</creatorcontrib><creatorcontrib>Kim, Woo-Sik</creatorcontrib><creatorcontrib>Jin, Seong-Deok</creatorcontrib><creatorcontrib>Koo, Tae Hyeon</creatorcontrib><creatorcontrib>Jang, Hye-Ock</creatorcontrib><creatorcontrib>Yun, Il</creatorcontrib><creatorcontrib>Kim, Kyu-Won</creatorcontrib><creatorcontrib>Bae, Moon-Kyoung</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Archives of pharmacal research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Park, Hyun-Joo</au><au>Jeong, Seong-Kyoon</au><au>Kim, Su-Ryun</au><au>Bae, Soo-Kyung</au><au>Kim, Woo-Sik</au><au>Jin, Seong-Deok</au><au>Koo, Tae Hyeon</au><au>Jang, Hye-Ock</au><au>Yun, Il</au><au>Kim, Kyu-Won</au><au>Bae, Moon-Kyoung</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Resveratrol inhibits Porphyromonas gingivalis lipopolysaccharide-induced endothelial adhesion molecule expression by suppressing NF-kappaB activation</atitle><jtitle>Archives of pharmacal research</jtitle><addtitle>Arch Pharm Res</addtitle><date>2009-04</date><risdate>2009</risdate><volume>32</volume><issue>4</issue><spage>583</spage><epage>591</epage><pages>583-591</pages><issn>0253-6269</issn><abstract>P. gingivalis is a major pathogen that is involved in the onset and progression of periodontal disease. 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subjects Animals
Anti-Inflammatory Agents - pharmacology
Cell Adhesion - drug effects
Dose-Response Relationship, Drug
Endothelial Cells - drug effects
Endothelial Cells - immunology
Humans
I-kappa B Proteins - metabolism
Intercellular Adhesion Molecule-1 - genetics
Intercellular Adhesion Molecule-1 - metabolism
Leukocytes - drug effects
Leukocytes - immunology
Lipopolysaccharides - isolation & purification
Lipopolysaccharides - pharmacology
Male
NF-KappaB Inhibitor alpha
Phosphorylation
Porphyromonas gingivalis - chemistry
Porphyromonas gingivalis - pathogenicity
Rats
Rats, Sprague-Dawley
RNA, Messenger - metabolism
Stilbenes - pharmacology
Transcription Factor RelA - metabolism
Transcription, Genetic - drug effects
U937 Cells
Vascular Cell Adhesion Molecule-1 - genetics
Vascular Cell Adhesion Molecule-1 - metabolism
title Resveratrol inhibits Porphyromonas gingivalis lipopolysaccharide-induced endothelial adhesion molecule expression by suppressing NF-kappaB activation
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