Abstract
Bone homeostasis is dynamically balanced between bone forming osteoblasts and bone resorbing osteoclasts. Osteoclasts play an important role in bone destruction and osteoporosis, and they are derived from monocyte/macrophages in response to macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor κB (NF-κB) ligand (RANKL). Amaranthus mangostanus L. (AM) is a plant with powerful antioxidant and other biological activities including anti-inflammatory, antidiabetic, and antihyperlipidemic effects. However, its effects on bone health are unknown. In this study, we explored whether AM could affect RANK-mediated osteoclastogenesis. AM significantly suppressed RANKL-induced osteoclast differentiation and expression of osteoclast-specific genes, TRAP, cathepsin K, NF-activated T-cells (NFATc1), and Dc-stamp in RAW 264.7 cells. Moreover, AM significantly inhibited extracellular signal-regulated kinase (ERK), Akt, and NF-κB signaling pathways in RAW 264.7 cells. In addition, AM preserved ovariectomy-induced bone loss in mice. Taken together, our results suggest that AM might be a potential candidate for the treatment of postmenopausal osteoporosis.
Highlights
Osteoporosis is a metabolic bone disease associated with low bone mass and microarchitectural failure of bone and increased risk of bone fractures
Binding of RANKL to RANK is a key factor for osteoclast differentiation and functions, and the resulting complex leads to the recruitment tumor necrosis factor (TNF) receptor-associated factors (TRAFs) and activates downstream signaling pathways, mainly nuclear factor κB (NF-κB), mitogen-activated protein kinase (MAPK), and AKT
To determine the effects of Amaranthus mangostanus L. (AM) on osteoclastogenesis, RAW 264.7 cells were incubated with RANKL in presence or absence of various concentrations of AM
Summary
Osteoporosis is a metabolic bone disease associated with low bone mass and microarchitectural failure of bone and increased risk of bone fractures. Binding of RANKL to RANK is a key factor for osteoclast differentiation and functions, and the resulting complex leads to the recruitment tumor necrosis factor (TNF) receptor-associated factors (TRAFs) and activates downstream signaling pathways, mainly NF-κB, mitogen-activated protein kinase (MAPK), and AKT. It activates transcription factors such as nuclear factor of activated T cells (NFATc1) and c-fos to induce osteoclastogenesis [6,7,8]. We investigated the preventive and therapeutic effects of AM on an ovariectomy(OVX-) induced bone loss in mice
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