Inflammatory responses of gingival epithelial cells stimulated with Porphyromonas gingivalis vesicles are inhibited by hop-associated polyphenols.
BACKGROUND
Periodontitis is induced by an imbalance between bacterial virulence and host defense ability. Porphyromonas gingivalis, a predominant periodontal pathogen, triggers a series of host inflammatory responses that aggravate the destruction of periodontium. Thus, anti-inflammatory reagents are considered desirable for effective periodontal therapy. In the present study, we examined the inhibitory effects of hop bract polyphenol (HBP) on cellular inflammatory responses induced by P. gingivalis membrane vesicles.


METHODS
Immortalized human gingival epithelial cells were stimulated with P. gingivalis membrane vesicles, and the effects of HBP on mRNA expression of cyclooxygenase (COX)-2, interleukin (IL)-6 and -8, and matrix metalloproteinase (MMP)-1 and -3 were examined using real-time reverse transcription-polymerase chain reaction.


RESULTS
HBP inhibited the mRNA expression of COX-2, IL-6 and -8, and MMP-1 and -3 in a dose-dependent manner, whereas epigallocatechin gallate (a control polyphenol) inhibited COX-2 mRNA expression only. Following further fractionation of HBP to identify the effective components, 2-[(2-methylpropanoyl)-phloroglucinol]1-O-beta-D-glucopyranoside (MPPG) was identified as a significant anti-inflammatory element that completely inhibited the inflammatory mRNA induction. Kaempferol 3-O-beta-glucopyranoside (astragalin) also was found to have anti-inflammatory effects.


CONCLUSIONS
HBP is suggested to be a potent inhibitor of cellular inflammatory responses induced by P. gingivalis vesicles. Further, MPPG and astragalin, identified here as effective components of HBP, also may be useful for the prevention and/or attenuation of periodontitis.
Kou
Yurong
Y
Department of Oral Frontier Biology, Osaka University Graduate School of Dentistry, Suita-Osaka, Japan.
Inaba
Hiroaki
H
Kato
Takahiro
T
Tagashira
Motoyuki
M
Honma
Daiki
D
Kanda
Tomomasa
T
Ohtake
Yasuyuki
Y
Amano
Atsuo
A
D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002461:Cell Line, Transformed; D002478:Cells, Cultured; D051546:Cyclooxygenase 2 / Q000187:drug effects; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology; D022162:Cytoplasmic Vesicles / Q000187:drug effects / Q000276:immunology*; D004305:Dose-Response Relationship, Drug; D004847:Epithelial Cells / Q000187:drug effects / Q000276:immunology / Q000382:microbiology; D005419:Flavonoids / Q000494:pharmacology*; D005881:Gingiva / Q000187:drug effects / Q000276:immunology / Q000382:microbiology*; D006801:Humans; D027582:Humulus; D016209:Interleukin-8 / Q000037:antagonists & inhibitors; D044949:Kaempferols / Q000494:pharmacology; D020781:Matrix Metalloproteinase 1; D019278:Matrix Metalloproteinase 3; D061965:Matrix Metalloproteinase Inhibitors; D010636:Phenols / Q000494:pharmacology*; D010696:Phloroglucinol / Q000031:analogs & derivatives / Q000494:pharmacology; D018515:Plant Leaves; D059808:Polyphenols; D016966:Porphyromonas gingivalis / Q000187:drug effects / Q000276:immunology*; D000093242:Interleukin-6 Inhibitors
D000893:Anti-Inflammatory Agents; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D005419:Flavonoids; D016209:Interleukin-8; D044949:Kaempferols; D020781:Matrix Metalloproteinase 1; D019278:Matrix Metalloproteinase 3; D061965:Matrix Metalloproteinase Inhibitors; D010636:Phenols; D010696:Phloroglucinol; D059808:Polyphenols; D000093242:Interleukin-6 Inhibitors; C456439:phlorin phloroglucinol; C001579:astragalin; C511768:MMP3 protein, human; C522360:MMP1 protein, human