title: Identification of hop polyphenolic components which inhibit prostaglandin E2 production by gingival epithelial cells stimulated with periodontal pathogen.
abstract: Chronic marginal periodontitis is a destructive inflammatory disease caused by an imbalance between bacterial virulence and host defense ability, resulting in eventual tooth exfoliation. Porphyromonas gingivalis, a major periodontal pathogen, triggers a series of cellular inflammatory responses including the production of prostaglandin E2 (PGE2), which causes periodontal destruction; thus, anti-inflammatory reagents are considered beneficial for periodontal therapy. In the present study, we examined whether hop- and apple-derived polyphenols (HBP and ACT, respectively) inhibit PGE2 production by human gingival epithelial (HGE) cells stimulated with P. gingivalis components. HGE cells were stimulated with P. gingivalis membrane vesicles, and the effects of HBP, ACT and epigallocatechin gallate (EGCg) on PGE2 production by HGE cells were evaluated using an enzyme-linked immunosorbent assay. HBP and EGCg significantly inhibited PGE2 production, whereas ACT did not. By further fractionation steps of HBP to identify the effective components, 3 components of HBP, 2-[(2-methylpropanoyl)-phloroglucinol]1-O-beta-D-glucopyranoside (MPPG), quercetin 3-O-beta-D-glucopyranoside (isoquercitrin), and kaempferol 3-O-beta-glucopyranoside (astragalin), were found to be elements which significantly inhibited cellular PGE2 production. These results suggest that HBP is a potent inhibitor of cellular PGE2 production induced by P. gingivalis, and HBP may be useful for the prevention and attenuation of periodontitis.
authors.affiliation: Department of Oral Frontier Biology, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka, Suita, Osaka 565-0871, Japan.
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Inaba
authors.forename: Motoyuki
authors.initials: M
authors.lastname: Tagashira
authors.forename: Daiki
authors.initials: D
authors.lastname: Honma
authors.forename: Tomomasa
authors.initials: T
authors.lastname: Kanda
authors.forename: Yurong
authors.initials: Y
authors.lastname: Kou
authors.forename: Yasuyuki
authors.initials: Y
authors.lastname: Ohtake
authors.forename: Atsuo
authors.initials: A
authors.lastname: Amano
mesh_terms: D002478:Cells, Cultured; D015232:Dinoprostone / Q000037:antagonists & inhibitors* / Q000096:biosynthesis; D004797:Enzyme-Linked Immunosorbent Assay; D004847:Epithelial Cells / Q000276:immunology / Q000382:microbiology; D005419:Flavonoids / Q000302:isolation & purification / Q000494:pharmacology*; D005881:Gingiva / Q000166:cytology / Q000382:microbiology*; D006801:Humans; D027582:Humulus / Q000737:chemistry*; D027845:Malus / Q000737:chemistry; D013058:Mass Spectrometry; D015394:Molecular Structure; D010636:Phenols / Q000302:isolation & purification / Q000494:pharmacology*; D059808:Polyphenols; D016966:Porphyromonas gingivalis / Q000472:pathogenicity*
chemical_list: D005419:Flavonoids; D010636:Phenols; D059808:Polyphenols; D015232:Dinoprostone