Abstract
Vanilloid receptor-1 (VR1) has been reported to exhibit multiple functions which can transduce painsensitive signals in nerve systems. A VR1 ligand, capsaicin ,h as been reported to show activities against inflammation an dc ancer growth, however, its role in bone metabolism is still unknown. Here, we examined the effect of capsaici no n cytokine-induced inflammatory bone resorption. Capsaicin suppressed interleukin-1-induced bone resorption in a mouse calvarial organex vivo culture in a dose-dependent manner. An assay using cocultures ofosteoblastsand bone marrow cells clearly showed the inhibition of osteoclast formation by treatment with capsaicin. Receptor activator of NF-κB ligand (RANKL), the sole inducer of osteoclast formation, is known to be produced by osteoblasts. In th ec ocultures o fb one marrow cells and osteoblasts, the expression of RANKL was suppressed by capsaicin. VR1 showed expression predominantly in osteoblasts, suggesting that capsaicin directly modulates osteoclast differentiation through the suppression of RANKL expression. VR1 ligands like capsaicin have the potential for use as clinical drugs targeting some bone diseases involving cytokine-induced bone resorption.
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