Journal
FRONTIERS IN ENDOCRINOLOGY
Volume 13, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fendo.2022.963237
Keywords
osteoclast; Gallic acid; Akt; ERK; JNK; osteoporosis
Categories
Funding
- National Natural Science Foundation of China
- Hangzhou Agricultural and Social Development Research Active Design Project
- [82105014]
- [82205136]
- [20180417A04]
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The study demonstrated that gallic acid (GA) can significantly inhibit osteoclast formation and function in osteoporosis by blocking multiple signaling pathways. Furthermore, it was shown to prevent bone loss in a mouse model. This suggests that GA could be a potential agent for the treatment of osteoporosis.
Osteoporosis is a common metabolic bone disease with a rapidly increasing prevalence, characterized by massive bone loss because of excessive osteoclast formation. Gallic acid (GA), a phenolic acid isolated from Cornus officinalis, has anti-inflammatory and anti-oxidant effects, but its effect on osteoclast formation has not been confirmed. In our study, we demonstrated that GA significantly inhibited RANKL-induced osteoclast formation and function of osteoclast in bone marrow monocytes (BMMs) and RAW264.7 cells in a dose-dependent manner without cytotoxicity. For molecular mechanisms, GA repressed osteoclastogenesis by blocking Akt, ERK, and JNK pathways, and suppressed osteoclastogenesis-related marker expression, including nuclear factor of the activated T-cell cytoplasmic 1 (NFATc1), c-Fos, and cathepsin K (CTSK). In addition, we further assessed the effect of GA in an ovariectomized mouse model, which indicated that GA has a notable effect on preventing bone loss. In conclusion, GA exerts notable effects in inhibiting osteoclastogenesis and preventing ovariectomy-induced bone loss, suggesting that GA is a potential agent in osteoporosis treatment.
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