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 |
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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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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.</description><identifier>ISSN: 0253-6269</identifier><identifier>DOI: 10.1007/s12272-009-1415-7</identifier><identifier>PMID: 19407977</identifier><language>eng</language><publisher>Korea (South)</publisher><subject>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</subject><ispartof>Archives of pharmacal research, 2009-04, Vol.32 (4), p.583-591</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19407977$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><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><title>Resveratrol inhibits Porphyromonas gingivalis lipopolysaccharide-induced endothelial adhesion molecule expression by suppressing NF-kappaB activation</title><title>Archives of pharmacal research</title><addtitle>Arch Pharm Res</addtitle><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.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Cell Adhesion - drug effects</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - immunology</subject><subject>Humans</subject><subject>I-kappa B Proteins - metabolism</subject><subject>Intercellular Adhesion Molecule-1 - genetics</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>Leukocytes - drug effects</subject><subject>Leukocytes - immunology</subject><subject>Lipopolysaccharides - isolation & purification</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Male</subject><subject>NF-KappaB Inhibitor alpha</subject><subject>Phosphorylation</subject><subject>Porphyromonas gingivalis - chemistry</subject><subject>Porphyromonas gingivalis - pathogenicity</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>RNA, Messenger - metabolism</subject><subject>Stilbenes - pharmacology</subject><subject>Transcription Factor RelA - metabolism</subject><subject>Transcription, Genetic - drug effects</subject><subject>U937 Cells</subject><subject>Vascular Cell Adhesion Molecule-1 - genetics</subject><subject>Vascular Cell Adhesion Molecule-1 - metabolism</subject><issn>0253-6269</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kM1O5DAQhH0A7cDsPgCXlU_cDP6NJ0dADIuEAK24jzpxZ-LFiY2dIOZBeF9GC9Sl1KVP1VIRciL4meDcnhchpZWM85oJLQyzB-SIS6NYJat6QY5L-ce5qowxP8hC1Jrb2toj8v4XyytmmHIM1I-9b_xU6GPMqd_lOMQRCt36cetfIfhCg08xxbAr0LY9ZO-Q-dHNLTqKo4tTj8FDoOB6LD6OdIgB2zkgxbeUsfzPmh0tc_o8xy29X7NnSAkuKbTT_s20Z36Sww5CwV9fviRP6-unqz_s7uHm9urijiWjLbPONJ2oVCetUxaavWq-4k2FHdRao5TOVoC60h1XoGXbmVqLFcqVbhVKq5bk9LM25fgyY5k2gy8thgAjxrlsKitWWhu1B39_gXMzoNuk7AfIu833juoDU5x45g</recordid><startdate>200904</startdate><enddate>200904</enddate><creator>Park, Hyun-Joo</creator><creator>Jeong, Seong-Kyoon</creator><creator>Kim, Su-Ryun</creator><creator>Bae, Soo-Kyung</creator><creator>Kim, Woo-Sik</creator><creator>Jin, Seong-Deok</creator><creator>Koo, Tae Hyeon</creator><creator>Jang, Hye-Ock</creator><creator>Yun, Il</creator><creator>Kim, Kyu-Won</creator><creator>Bae, Moon-Kyoung</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200904</creationdate><title>Resveratrol inhibits Porphyromonas gingivalis lipopolysaccharide-induced endothelial adhesion molecule expression by suppressing NF-kappaB activation</title><author>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</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p547-7d5bf163f27d37abbbb9080b6efa944e22d76ae464f03a42cf59418e284c3e273</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Cell Adhesion - drug effects</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - immunology</topic><topic>Humans</topic><topic>I-kappa B Proteins - metabolism</topic><topic>Intercellular Adhesion Molecule-1 - genetics</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>Leukocytes - drug effects</topic><topic>Leukocytes - immunology</topic><topic>Lipopolysaccharides - isolation & 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. 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.</abstract><cop>Korea (South)</cop><pmid>19407977</pmid><doi>10.1007/s12272-009-1415-7</doi><tpages>9</tpages></addata></record> |
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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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