| Autor: |
ANG, ESTABELLE S. M., PAVLOS, NATHAN J., CHAI, LEE Y., QI, MING, CHENG, TAK S., STEER, JAMES H., JOYCE, DAVID A., ZHENG, MING H., XU, JIAKE |
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| Zdroj: |
Journal of Cellular Physiology; Dec2009, Vol. 221 Issue 3, p642-649, 8p, 7 Graphs |
| Abstrakt: |
Receptor activator NF-κB ligand (RANKL)-activated signaling is essential for osteoclast differentiation, activation and survival. Caffeic acid phenethyl ester (CAPE), a natural NF-κB 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 µM) 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-κB and NFAT activation, concomitant with delayed IκBα 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-κB 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. © 2009 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR] |
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