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 PGE 2 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-β-D-glucopyranoside (MPPG), quercetin 3-O-β-D-glucopyranoside (isoquercitrin), and kaempferol 3-O-β-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.
| Original language | English |
|---|---|
| Pages (from-to) | 527-530 |
| Number of pages | 4 |
| Journal | Biological and Pharmaceutical Bulletin |
| Volume | 31 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - Mar 2008 |
| Externally published | Yes |
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Keywords
- Gingival epithelial cell
- Hop bract polyphenol
- Humulus lupulus L.
- Porphyromonas gingivalis
- Prostaglandin E
ASJC Scopus subject areas
- Molecular Medicine
- Pharmacology, Toxicology and Pharmaceutics(all)
Cite this
Identification of hop polyphenolic components which inhibit prostaglandin E2 production by gingival epithelial cells stimulated with periodontal pathogen. / Inaba, Hiroaki; Tagashira, Motoyuki; Honma, Daiki; Kanda, Tomomasa; Kou, Yurong; Ohtake, Yasuyuki; Amano, Atsuo.
In: Biological and Pharmaceutical Bulletin, Vol. 31, No. 3, 03.2008, p. 527-530.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Identification of hop polyphenolic components which inhibit prostaglandin E2 production by gingival epithelial cells stimulated with periodontal pathogen
AU - Inaba, Hiroaki
AU - Tagashira, Motoyuki
AU - Honma, Daiki
AU - Kanda, Tomomasa
AU - Kou, Yurong
AU - Ohtake, Yasuyuki
AU - Amano, Atsuo
PY - 2008/3
Y1 - 2008/3
N2 - 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 PGE 2 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-β-D-glucopyranoside (MPPG), quercetin 3-O-β-D-glucopyranoside (isoquercitrin), and kaempferol 3-O-β-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.
AB - 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 PGE 2 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-β-D-glucopyranoside (MPPG), quercetin 3-O-β-D-glucopyranoside (isoquercitrin), and kaempferol 3-O-β-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.
KW - Gingival epithelial cell
KW - Hop bract polyphenol
KW - Humulus lupulus L.
KW - Porphyromonas gingivalis
KW - Prostaglandin E
UR - http://www.scopus.com/inward/record.url?scp=41149135325&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=41149135325&partnerID=8YFLogxK
U2 - 10.1248/bpb.31.527
DO - 10.1248/bpb.31.527
M3 - Article
C2 - 18310924
AN - SCOPUS:41149135325
VL - 31
SP - 527
EP - 530
JO - Biological and Pharmaceutical Bulletin
JF - Biological and Pharmaceutical Bulletin
SN - 0918-6158
IS - 3
ER -