TY - JOUR
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
PY - 2008/1
Y1 - 2008/1
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.
KW - Kaempferol
KW - Periodontitis
KW - Phloroglucinol
KW - Porphyromonas gingivalis
UR - http://www.scopus.com/inward/record.url?scp=38549180700&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=38549180700&partnerID=8YFLogxK
U2 - 10.1902/jop.2008.070364
DO - 10.1902/jop.2008.070364
M3 - Article
C2 - 18166108
AN - SCOPUS:38549180700
SN - 0022-3492
VL - 79
SP - 174
EP - 180
JO - Journal of Periodontology
JF - Journal of Periodontology
IS - 1
ER -