Abstract
The rhizome of Atractylodes macrocephala has been used mainly in Traditional Chinese Medicine for invigorating the functions of the stomach and spleen. In the present study, we investigated the inhibitory effect of the 70% ethanol extract of the rhizome of Atractylodes macrocephala (AMEE) on osteoclast differentiation. We found that AMEE inhibits osteoclast differentiation from its precursors induced by receptor activator of nuclear factor-κB ligand (RANKL), an essential cytokine required for osteoclast differentiation. AMEE attenuated RANKL-induced activation of NF-κB signaling pathway, subsequently inhibiting the induction of osteoclastogenic transcription factors, c-Fos and nuclear factor of activated T cells cytoplasmic 1. Consistent with the in vitro results, administration of AMEE protected RANKL-induced bone loss in mice. We also identified atractylenolide I and II as active constituents contributing to the anti-osteoclastogenic effect of AMEE. Taken together, our results demonstrate that AMEE has a protective effect on bone loss via inhibiting osteoclast differentiation and suggest that AMEE may be useful in preventing and treating various bone diseases associated with excessive bone resorption.
Highlights
Osteoporosis, a metabolic disease characterized by low bone mass and microarchitectural deterioration of bone tissue, is a major health problem of aging population, especially in postmenopausal women [1]
RANKL binding to its receptor RANK on the cell surface of osteoclast precursors induces the recruitment of adaptor molecules such as tumor necrosis factor receptor-associated factor 6, which stimulates the activation of mitogen activated protein (MAP) kinases and transcription factors including NF-κB, c-Fos, and nuclear factor of activated T cells cytoplasmic 1 (NFATc1) [5,6]
We investigated whether AMEE inhibits osteoclast differentiation in bone marrow cell-osteoblast coculture system, in which calciotropic factors such as 1α,25-dihydroxyvitaminD3 (VitD3) and IL-1 promote osteoclast differentiation from bone marrow cells by increasing RANKL expression and/or decreasing its decoy receptor osteoprotegerin (OPG) expression in osteoblasts [2]
Summary
Osteoporosis, a metabolic disease characterized by low bone mass and microarchitectural deterioration of bone tissue, is a major health problem of aging population, especially in postmenopausal women [1]. RANKL binding to its receptor RANK on the cell surface of osteoclast precursors induces the recruitment of adaptor molecules such as tumor necrosis factor receptor-associated factor 6, which stimulates the activation of mitogen activated protein (MAP) kinases and transcription factors including NF-κB, c-Fos, and nuclear factor of activated T cells cytoplasmic 1 (NFATc1) [5,6]. These transcription factors play a crucial role in osteoclast differentiation [7,8,9]. Its bone protective effect was evaluated in a murine model of bone loss by RANKL injection
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