Inflammatory responses of gingival epithelial cells stimulated with porphyromonas gingivalis vesicles are inhibited by hop-associated polyphenols

Yurong Kou, Hiroaki Inaba, Takahiro Kato, Motoyuki Tagashira, Daiki Honma, Tomomasa Kanda, Yasuyuki Ohtake, Atsuo Amano

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

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 mRMA 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-β-D-glucopyranoside (MPPG) was identified as a significant anti-inflammatory element that completely inhibited the inflammatory mRNA induction. Kaempferol 3-O-β-glucopyranoside (astragalin) also was found to have antiinflammatory 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.

Original languageEnglish
Pages (from-to)174-180
Number of pages7
JournalJournal of Periodontology
Volume79
Issue number1
DOIs
Publication statusPublished - Jan 2008
Externally publishedYes

Fingerprint

Humulus
Porphyromonas gingivalis
Polyphenols
Epithelial Cells
Cyclooxygenase 2
Phloroglucinol
Matrix Metalloproteinase 3
Matrix Metalloproteinase 1
Anti-Inflammatory Agents
Periodontitis
Interleukin-8
Messenger RNA
Interleukin-6
Periodontium
Membranes
Reverse Transcription
Virulence
Polymerase Chain Reaction

Keywords

  • Kaempferol
  • Periodontitis
  • Phloroglucinol
  • Porphyromonas gingivalis

ASJC Scopus subject areas

  • Dentistry(all)

Cite this

Inflammatory responses of gingival epithelial cells stimulated with porphyromonas gingivalis vesicles are inhibited by hop-associated polyphenols. / Kou, Yurong; Inaba, Hiroaki; Kato, Takahiro; Tagashira, Motoyuki; Honma, Daiki; Kanda, Tomomasa; Ohtake, Yasuyuki; Amano, Atsuo.

In: Journal of Periodontology, Vol. 79, No. 1, 01.2008, p. 174-180.

Research output: Contribution to journalArticle

Kou, Yurong ; Inaba, Hiroaki ; Kato, Takahiro ; Tagashira, Motoyuki ; Honma, Daiki ; Kanda, Tomomasa ; Ohtake, Yasuyuki ; Amano, Atsuo. / Inflammatory responses of gingival epithelial cells stimulated with porphyromonas gingivalis vesicles are inhibited by hop-associated polyphenols. In: Journal of Periodontology. 2008 ; Vol. 79, No. 1. pp. 174-180.
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T1 - Inflammatory responses of gingival epithelial cells stimulated with porphyromonas gingivalis vesicles are inhibited by hop-associated polyphenols

AU - Kou, Yurong

AU - Inaba, Hiroaki

AU - Kato, Takahiro

AU - Tagashira, Motoyuki

AU - Honma, Daiki

AU - Kanda, Tomomasa

AU - Ohtake, Yasuyuki

AU - Amano, Atsuo

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N2 - 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 mRMA 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-β-D-glucopyranoside (MPPG) was identified as a significant anti-inflammatory element that completely inhibited the inflammatory mRNA induction. Kaempferol 3-O-β-glucopyranoside (astragalin) also was found to have antiinflammatory 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.

AB - 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 mRMA 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-β-D-glucopyranoside (MPPG) was identified as a significant anti-inflammatory element that completely inhibited the inflammatory mRNA induction. Kaempferol 3-O-β-glucopyranoside (astragalin) also was found to have antiinflammatory 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.

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