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

Arch Pharm Res. 2009 Apr;32(4):583-91. doi: 10.1007/s12272-009-1415-7. Epub 2009 Apr 29.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 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*
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Resveratrol
  • Stilbenes / pharmacology*
  • Transcription Factor RelA / metabolism*
  • Transcription, Genetic / drug effects
  • U937 Cells
  • Vascular Cell Adhesion Molecule-1 / genetics
  • Vascular Cell Adhesion Molecule-1 / metabolism*

Substances

  • Anti-Inflammatory Agents
  • I-kappa B Proteins
  • Lipopolysaccharides
  • NFKBIA protein, human
  • Nfkbia protein, rat
  • RELA protein, human
  • RNA, Messenger
  • Stilbenes
  • Transcription Factor RelA
  • Vascular Cell Adhesion Molecule-1
  • Intercellular Adhesion Molecule-1
  • NF-KappaB Inhibitor alpha
  • Resveratrol