Hydroxychavicol Inhibits In Vitro Osteoclastogenesis via the Suppression of NF-κB Signaling Pathway
1
Issued Date
2024-01-01
Resource Type
ISSN
19769148
eISSN
20054483
Scopus ID
2-s2.0-85186397102
Journal Title
Biomolecules and Therapeutics
Volume
32
Issue
2
Start Page
205
End Page
213
Rights Holder(s)
SCOPUS
Bibliographic Citation
Biomolecules and Therapeutics Vol.32 No.2 (2024) , 205-213
Suggested Citation
Srihirun S., Mathithiphark S., Phruksaniyom C., Kongphanich P., Inthanop W., Sriwantana T., Tancharoen S., Sibmooh N., Vivithanaporn P. Hydroxychavicol Inhibits In Vitro Osteoclastogenesis via the Suppression of NF-κB Signaling Pathway. Biomolecules and Therapeutics Vol.32 No.2 (2024) , 205-213. 213. doi:10.4062/biomolther.2023.067 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/97537
Title
Hydroxychavicol Inhibits In Vitro Osteoclastogenesis via the Suppression of NF-κB Signaling Pathway
Corresponding Author(s)
Other Contributor(s)
Abstract
Hydroxychavicol, a primary active phenolic compound of betel leaves, previously inhibited bone loss in vivo by stimulating os-teogenesis. However, the effect of hydroxychavicol on bone remodeling induced by osteoclasts is unknown. In this study, the anti-osteoclastogenic effects of hydroxychavicol and its mechanism were investigated in receptor activator of nuclear factor kap-pa-B ligand (RANKL)-induced osteoclasts. Hydroxychavicol reduced the number of tartrate resistance acid phosphatase (TRAP)-positive multinucleated, F-actin ring formation and bone-resorbing activity of osteoclasts differentiated from RAW264.7 cells in a concentration-dependent manner. Furthermore, hydroxychavicol decreased the expression of osteoclast-specific genes, including cathepsin K, MMP-9, and dendritic cell-specific transmembrane protein (DC-STAMP). For mechanistic studies, hydroxychavicol suppressed RANKL-induced expression of major transcription factors, including the nuclear factor of activated T-cells 1 (NFATc1), c-Fos, and c-Jun. At the early stage of osteoclast differentiation, hydroxychavicol blocked the phosphorylation of NF-κB subunits (p65 and Iκβα). This blockade led to the decrease of nuclear translocation of p65 induced by RANKL. In addition, the anti-osteo-clastogenic effect of hydroxychavicol was confirmed by the inhibition of TRAP-positive multinucleated differentiation from human peripheral mononuclear cells (PBMCs). In conclusion, hydroxychavicol inhibits osteoclastogenesis by abrogating RANKL-induced NFATc1 expression by suppressing the NF-κB signaling pathway in vitro.