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

• Published in: Journal of microbiology and biotechnology Vol. 28; no. 8; pp. 1270 - 1281
• Main Authors: Kim, Siyeon, Kook, Kyo Eun, Kim, Changhee, Hwang, Jae-Kwan
• Format: Journal Article
• Language: English
• Published: Korea (South) 한국미생물·생명공학회 28.08.2018
• Subjects: Animals; Anti-Inflammatory Agents - chemistry; Anti-Inflammatory Agents - pharmacology; Cell Line; Cell Survival - drug effects; Curcuma - chemistry; Fibroblasts - immunology; Gene Expression - drug effects; Humans; Inflammation - genetics; Lipopolysaccharides - adverse effects; MAP Kinase Signaling System - drug effects; Mice; Molecular Structure; Osteoclasts - cytology; Osteoclasts - drug effects; Osteogenesis - drug effects; Phenols - chemistry; Phenols - pharmacology; Plant Extracts - chemistry; Plant Extracts - pharmacology; RANK Ligand - metabolism; RAW 264.7 Cells; 생물학; xanthorrhizol; osteoclastogenesis; Curcuma xanthorrhiza; gingival inflammation; periodontitis
• ISSN: 1017-7825; 1738-8872
• DOI: 10.4014/jmb.1803.03045

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 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 MAPK/AP-1 pathway.