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Binding of RANKL with RANK on the surface of osteoclasts triggers the release of the endothelial cytokine TNF receptor-associated factor 6 (TRAF 6) in the cytoplasm that activates various signaling pathways in the precursor cells, including the mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase/AKT (PI3K/AKT) and nuclear factor kappa B (NF-κB) pathways. 7 RANKL secreted by osteoblasts belongs to the tumor necrosis factor (TNF) super family. 4 During differentiation, a unique ring is formed by the actin cytoskeleton at the contact location of bones to ensure the integrity of the osteoclast structure. 6 M-CSF is involved in the survival and division of bone marrow-derived mononuclear macrophages, whereas RANKL promotes the fusion of osteoclast precursor cells and differentiation into the lineage of osteoclasts.
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5 The differentiation and formation of osteoclast precursor cells are governed by two important factors, namely, receptor activator of nuclear factor kappa B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). 4 Bone abnormalities caused by postmenopausal osteoporosis, rheumatoid arthritis, periodontitis and other bone diseases are closely related to the overactivity of osteoclasts. 2, 3 Excessive osteoclast activity can lead to osteoporosis. 1 Bone homeostasis involves sustaining a balance between bone formation of osteoblasts and bone resorption of osteoclasts. Osteoclasts, a type of giant multinucleated cells are derived from the macrophage/mononuclear lineage in the bone marrow. Keywords: saikosaponin D, osteoclastogenesis, NF-κB, MAPKs, PI3K-AKT, therapy SSD suppressed LPS-induced inflammatory bone loss in vivo.Ĭonclusion: SSD inhibited osteoclastogenesis and LPS-induced osteolysis in mice both which served as a new potential agent for the treatment of osteoclast-related conditions. Results: SSD inhibited the formation and bone resorption of osteoclasts induced by RANKL in vitro. The excised calvaria bones were used for TRAP staining, micro-CT scan and histological analysis. A mouse model of LPS-induced calvarial bone loss was established and treated with different doses of SSD. TRAP staining, bone resorption determination, qRT-PCR, immunofluorescence and Western blotting were performed. Methods: BMMs were cultured in complete medium stimulated by RANKL with different concentrations of SSD. Purpose: To explore whether SSD could prevent osteoclast differentiation and bone resorption induced by M-CSF and RANKL, and further evaluate the potential therapeutic properties of SSD in LPS-induced inflammatory bone loss mouse models. However, the role of SSD in regulating the differentiation and function of osteoclasts is not clear. Saikosaponin D (SSD) is the active extract of Bupleurum, which has anti-inflammation, anti-tumor and liver protection functions. Considering the complications and other limitations of current drug treatments, it is necessary to develop a safer and more reliable drug to deal with osteoclast-related diseases. *These authors contributed equally to this workĭepartment of Orthopedics, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Linhai, 317000, People’s Republic of Chinaīackground: Osteolytic diseases such as osteoporosis are featured with accelerated osteoclast differentiation and strong bone resorption. Xinhui Wu, 1, 2, * Kangxian Zhao, 1, 2, * Xiaoxin Fang, 3, 4 Feng Lu, 3, 4 Weikang Zhang, 1, 2 Xiaoting Song, 1, 2 Lihua Chen, 5 Jiacheng Sun, 1, 2 Haixiao Chen 1, 2, 4ġWenzhou Medical University, Wenzhou, People’s Republic of China 2Department of Orthopedics, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Linhai, People’s Republic of China 3Zhejiang University School of Medicine, Hangzhou, People’s Republic of China 4Taizhou Hospital of Zhejiang Province, Zhejiang University, Linhai, People’s Republic of China 5Enze Medical Research Center, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Linhai, People’s Republic of China