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
School of Dentistry, Pusan National University, Pusan, 602-739, Korea.
Arch Pharm Res. 2009 Apr;32(4):583-91. doi: 10.1007/s12272-009-1415-7. Epub 2009 Apr 29.
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.
牙龈卟啉单胞菌是参与牙周病发生和发展的主要病原体。本研究调查了天然存在的多酚白藜芦醇对牙龈卟啉单胞菌脂多糖加速的血管炎症的影响，这是牙周炎进展中的关键步骤。白藜芦醇通过下调细胞黏附分子ICAM-1和VCAM-1，显著抑制牙龈卟啉单胞菌脂多糖诱导的白细胞与内皮细胞及主动脉内皮的黏附。此外，白藜芦醇对牙龈卟啉单胞菌脂多糖诱导的细胞黏附分子的抑制作用主要由核因子-κB（NF-κB）介导。白藜芦醇抑制了牙龈卟啉单胞菌脂多糖刺激的人微血管内皮细胞中IκBα磷酸化及NF-κB p65亚基的核转位。总体而言，这些发现表明白藜芦醇通过抑制NF-κB依赖性细胞黏附分子的表达，显著减轻牙龈卟啉单胞菌脂多糖诱导的单核细胞与内皮的黏附，提示其在牙周病原体诱导的血管炎症中的治疗作用。
