2018 ; Vol.28-8: 1270~1281
|Author||Siyeon Kim, Kyo Eun Kook, Changhee Kim, Jae-Kwan Hwang|
|Place of duty||Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, Republic of Korea|
|Title||Inhibitory Effects of Curcuma xanthorrhiza Supercritical Extract and Xanthorrhizol on LPS-Induced Inflammation in HGF-1 Cells and RANKL-Induced Osteoclastogenesis in RAW264.7 Cells|
J. Microbiol. Biotechnol.2018 ;
|Abstract||Periodontal disease is triggered by the host immune response to pathogens in the microbial
biofilm. Worsening of periodontal disease destroys the tooth-supporting tissues and alveolar
bone. As oral inflammation can induce systemic diseases in humans, it is important to prevent
periodontal disease. In this study, we demonstrated that Curcuma xanthorrhiza supercritical
extract (CXS) and its active compound, xanthorrhizol (XAN), exhibit anti-inflammatory effects
on lipopolysaccharide (LPS)-treated human gingival fibroblast-1 cells and anti-osteoclastic
effects on receptor activator of nuclear factor kappa B ligand (RANKL)-treated RAW264.7
cells. LPS-upregulated inflammatory factors, such as nuclear factor kappa B p65 and
interleukin-1β, were prominently reduced by CXS and XAN. In addition, RANKL-induced
osteoclastic factors, such as nuclear factor of activated T-cells c1, tartrate-resistant acid
phosphatase, and cathepsin K, were decreased in the presence of CXS and XAN. CXS and
XAN inhibited the mitogen-activated protein kinase (MAPK)/activator protein-1 (AP-1)
signaling pathway. Collectively, these results provide evidence that CXS and XAN suppress
LPS-induced inflammation and RANKL-induced osteoclastogenesis by suppressing the
|Key_word||Curcuma xanthorrhiza, Xanthorrhizol, gingival Inflammation, osteoclastogenesis, periodontitis|
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