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Inhibitory effect of oolonghomobisflavan B on osteoclastogenesis by suppressing p38 MAPK activation
Soomin Lim1, Tae Hoon Kim2, Hye Jung Ihn3
1Department of Oral Pathology and Regenerative Medicine, School of Dentistry, IHBR, Kyungpook National University, Daegu 41940, Republic of Korea.
Abstract:
Suppression of differentiation and/or function of osteoclasts is considered an effective therapeutic strategy for osteolytic bone diseases such as periodontitis and osteoporosis. Evidence regarding the health benefits of oolong tea consumption is accumulating, and tea polyphenols have various pharmacological properties such as anti-cancer and anti-diabetes effects. In this study, we investigated the effect of oolonghomobisflavan B (OFB), a polyphenolic compound in oolong tea, on osteoclast differentiation. OFB suppressed receptor activator of nuclear factor-κB (RANKL)-induced formation of tartate-resistant acid phosphatase-positive multinuclear cells without cytotoxicity. OFB also significantly attenuated p38 phosphorylation, which is essential for RANKL-induced osteoclastogenesis, and inhibited the expressions of nuclear factor of activated T cells, cytoplasmic 1 (NFATc1) and osteoclast-specific target genes, including dendritic cell-specific transmembrane protein and cathepsin K. Our findings suggest that OFB exhibits an anti-osteoclastogenic activity by inhibiting RANKL-mediated p38 activation, which is useful for the prevention and treatment of osteolytic bone diseases.
Insights
Oolonghomobisflavan B, a compound in oolong tea, effectively inhibits osteoclast differentiation. This suggests OFB may be beneficial for treating osteolytic bone diseases like osteoporosis and periodontitis.
Area of Science:
- Biochemistry
- Pharmacology
- Bone Biology
Background:
- Osteoclast differentiation is a therapeutic target for osteolytic bone diseases.
- Oolong tea polyphenols possess various pharmacological properties.
- Oolonghomobisflavan B (OFB) is a key polyphenol in oolong tea.
Purpose of the Study:
- To investigate the effect of OFB on osteoclast differentiation.
- To explore the molecular mechanisms underlying OFB's action on osteoclasts.
Main Methods:
- Assessing OFB's effect on receptor activator of nuclear factor-κB (RANKL)-induced osteoclast formation.
- Evaluating OFB's impact on p38 phosphorylation, a critical pathway in osteoclastogenesis.
- Measuring the expression of key osteoclast-specific genes, including NFATc1, DC-STAMP, and cathepsin K.
Main Results:
- OFB suppressed RANKL-induced osteoclast formation without cytotoxicity.
- OFB significantly attenuated p38 phosphorylation.
- OFB inhibited the expression of NFATc1 and osteoclast-specific genes like DC-STAMP and cathepsin K.
Conclusions:
- OFB demonstrates anti-osteoclastogenic activity.
- OFB inhibits osteoclast differentiation by suppressing RANKL-mediated p38 activation.
- OFB holds potential for preventing and treating osteolytic bone diseases.
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