Journal of Microbiology and Biotechnology

The Korean Society for Microbiology and Biotechnology (한국미생물·생명공학회)
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Inhibitory Effects of Panduratin A on Periodontitis-Induced Inflammation and Osteoclastogenesis through Inhibition of MAPK Pathways In Vitro

  • Kim, Haebom (Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University) ;
  • Kim, Mi-Bo (Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University) ;
  • Kim, Changhee (Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University) ;
  • Hwang, Jae-Kwan (Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University)
  • Received : 2017.07.18
  • Accepted : 2017.10.18
  • Published : 2018.02.28
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Abstract

Periodontitis is an inflammatory disease caused by microbial lipopolysaccharide (LPS), destroying gingival tissues and alveolar bone in the periodontium. In the present study, we evaluated the anti-inflammatory and anti-osteoclastic effects of panduratin A, a chalcone compound isolated from Boesenbergia pandurata, in human gingival fibroblast-1 (HGF-1) and RAW 264.7 cells. Treatment of panduratin A to LPS-stimulated HGF-1 significantly reduced the expression of interleukin-$1{\beta}$ and nuclear factor-kappa B (NF-${\kappa}B$), subsequently leading to the inhibition of matrix metalloproteinase-2 (MMP-2) and MMP-8 compared with that in the LPS control ($^{**}p$ < 0.01). These anti-inflammatory responses were mediated by suppressing the mitogen-activated protein kinase (MAPK) signaling and activator protein-1 complex formation pathways. Moreover, receptor activator of NF-${\kappa}B$ ligand (RANKL)-stimulated RAW 264.7 cells treated with panduratin A showed significant inhibition of osteoclastic transcription factors such as nuclear factor of activated T-cells c1 and c-Fos as well as osteoclastic enzymes such as tartrate-resistant acid phosphatase and cathepsin K compared with those in the RANKL control ($^{**}p$ < 0.01). Similar to HGF-1, panduratin A suppressed osteoclastogenesis by controlling MAPK signaling pathways. Taken together, these results suggest that panduratin A could be a potential candidate for development as a natural anti-periodontitis agent.

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References

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