title: Resveratrol inhibits Porphyromonas gingivalis lipopolysaccharide-induced endothelial adhesion molecule expression by suppressing NF-kappaB activation.
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.
authors.affiliation: School of Dentistry, Pusan National University, Pusan, 602-739, Korea.
authors.forename: Hyun-Joo
authors.initials: HJ
authors.lastname: Park
authors.forename: Seong-Kyoon
authors.initials: SK
authors.lastname: Jeong
authors.forename: Su-Ryun
authors.initials: SR
authors.lastname: Kim
authors.forename: Soo-Kyung
authors.initials: SK
authors.lastname: Bae
authors.forename: Woo-Sik
authors.initials: WS
authors.lastname: Kim
authors.forename: Seong-Deok
authors.initials: SD
authors.lastname: Jin
authors.forename: Tae Hyeon
authors.initials: TH
authors.lastname: Koo
authors.forename: Hye-Ock
authors.initials: HO
authors.lastname: Jang
authors.forename: Il
authors.initials: I
authors.lastname: Yun
authors.forename: Kyu-Won
authors.initials: KW
authors.lastname: Kim
authors.forename: Moon-Kyoung
authors.initials: MK
authors.lastname: Bae
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002448:Cell Adhesion / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D042783:Endothelial Cells / Q000187:drug effects* / Q000276:immunology; D006801:Humans; D020672:I-kappa B Proteins / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism*; D007962:Leukocytes / Q000187:drug effects / Q000276:immunology; D008070:Lipopolysaccharides / Q000302:isolation & purification / Q000494:pharmacology*; D008297:Male; D000072000:NF-KappaB Inhibitor alpha; D010766:Phosphorylation; D016966:Porphyromonas gingivalis / Q000737:chemistry / Q000472:pathogenicity*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D000077185:Resveratrol; D013267:Stilbenes / Q000494:pharmacology*; D051996:Transcription Factor RelA / Q000378:metabolism*; D014158:Transcription, Genetic / Q000187:drug effects; D020298:U937 Cells; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism*
chemical_list: D000893:Anti-Inflammatory Agents; D020672:I-kappa B Proteins; D008070:Lipopolysaccharides; C000606204:NFKBIA protein, human; C000606206:Nfkbia protein, rat; C498143:RELA protein, human; D012333:RNA, Messenger; D013267:Stilbenes; D051996:Transcription Factor RelA; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D000072000:NF-KappaB Inhibitor alpha; D000077185:Resveratrol