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Caffeic acid 3,4-dihydroxy-phenethyl ester suppresses receptor activator of NF-κB ligand–induced osteoclastogenesis and prevents ovariectomy-induced bone loss through inhibition of mitogen-activated protein kinase/activator protein 1 and Ca2+–nuclear factor of activated T-cells cytoplasmic 1 signaling pathways
Caffeic acid 3,4-dihydroxy-phenethyl ester reduces bone-destroying cell formation and prevents bone loss after ovary removal by blocking key cell signaling pathways
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Abstract
Caffeic acid 3,4-dihydroxy-phenethyl ester (CADPE) suppressed RANKL-induced osteoclast differentiation in mouse cells.
- CADPE inhibited osteoclast differentiation and actin-ring formation in mouse bone marrow monocytes and RAW264.7 cells in a dose-dependent manner.
- No effect of CADPE was observed on macrophage colony-stimulating factor-induced proliferation and differentiation.
- CADPE reduced RANKL-induced phosphorylation of key signaling proteins involved in osteoclastogenesis, including ERK1/2, p38, and JNK.
- Inhibition of nuclear translocation and activation of c-Fos by CADPE was noted, with overexpression of c-Fos counteracting CADPE's inhibitory effects.
- CADPE also blocked RANKL-induced interactions and signaling downstream of TRAF6 and prevented Ca2+ oscillations.
- In vivo, CADPE prevented bone loss in ovariectomized mice by inhibiting osteoclast activity.
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