Journal
JOURNAL OF CELLULAR PHYSIOLOGY
Volume 221, Issue 3, Pages 642-649Publisher
WILEY
DOI: 10.1002/jcp.21898
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Funding
- National Health and Medical Research Council of Australia
- Arthritis Foundation of Western Australia
- Sir Charles Gairdner Hospital (Perth, Western Australia) Research Fund
- University of Western Australia
- National Health and Medical Research Council of Australia (NHMRC)/Osteoporosis Australia Scholarship
- NHMRC (C.J. Martin) Overseas Biomedical Fellowship
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Receptor activator NF-kappa B ligand (RANKL)-activated signaling is essential for osteoclast differentiation, activation and survival. Caffeic acid phenethyl ester (CAPE), a natural NF-kappa B inhibitor from honeybee propolis has been shown to have anti-tumor and anti-inflammatory properties. In this study, we investigated the effect of CAPE on the regulation of RANKL-induced osteoclastogenesis, bone resorption and signaling pathways. Low concentrations of CAPE (< 1 mu M) dose dependently inhibited RANKL-induced osteoclastogenesis in RAW264.7 cell and bone marrow macrophage (BMM) cultures, as well as decreasing the capacity of human osteoclasts to resorb bone. CAPE inhibited both constitutive and RANKL-induced NF-kappa B and NFAT activation, concomitant with delayed I kappa B alpha degradation and inhibition of p65 nuclear translocation. At higher concentrations, CAPE induced apoptosis and caspase 3 activities of RAW264.7 and disrupts the microtubule network in osteoclast like (OCL) cells. Taken together, our findings demonstrate that inhibition of NF-kappa B and NFAT activation by CAPE results in the attenuation of osteoclastogenesis and bone resorption, implying that CAPE is a potential treatment for osteolytic bone diseases. J. Cell. Physiol. 221: 642-649, 2009. (C) 2009 Wiley-Liss, Inc.
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