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

• DOI: 10.1007/s12272-009-1415-7
• Publication Date: 2009-04-28T03:38:20Z
• Authors: Hyun-Joo Park; Seong-Kyoon Jeong; Su-Ryun Kim; Soo-Kyung Bae; Woo-Sik Kim; Seong-Deok Jin; Tae Hyeon Koo; Hye-Ock Jang; Il Yun; Kyu-Won Kim; Moon-Kyoung Bae
• Keywords: Lipopolysaccharides; Male; 0301 basic medicine; Dose-Response Relationship, Drug; Anti-Inflammatory Agents; Transcription Factor RelA; Endothelial Cells; Intercellular Adhesion Molecule-1; Rats; 3. Good health; Rats, Sprague-Dawley; 03 medical and health sciences; NF-KappaB Inhibitor alpha; Resveratrol; Stilbenes; Cell Adhesion; Leukocytes; Animals; Humans; I-kappa B Proteins; RNA, Messenger; Phosphorylation; Porphyromonas gingivalis

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.