Triterpenoid Saponin W3 from <i>Anemone flaccida</i> Suppresses Osteoclast Differentiation through Inhibiting Activation of MAPKs and NF-κB Pathways

Kong, Xiangying; Yang, Yanqi; Wu, Wenbin; Wan, Heng; Li, Xiaomin; Zhong, Michun; Su, Xiaohui; Jia, Shiwei; Lin, Na

doi:10.7150/ijbs.12296

Cited by 27 publications

(24 citation statements)

References 28 publications

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“…Osteoclasts are derived from osteoclast precursor cells (OPCs), which originate from the monocyte/macrophage lineage. Previous studies have demonstrated that the osteoblast-associated synthesis and secretion of receptor activator of nuclear factor κB ligand (RANKL) and osteoclast-associated RANK are essential in osteoclastogenesis, and that RANK on monocytes binds to RANKL, initiating osteoclast differentiation ( 4 , 5 ). Furthermore, macrophage-derived proinflammatory mediators in RA directly contribute to the degradation of articular cartilage and subchondral bone, and the activation of RA monocytes/macrophages occurs locally and in the peripheral circulation ( 6 , 7 ).…”

Section: Introductionmentioning

confidence: 99%

Curcumin inhibits osteoclastogenic potential in PBMCs from rheumatoid arthritis patients via the suppression of MAPK/RANK/c-Fos/NFATc1 signaling pathways

Shang

Zhao

Dong

et al. 2016

Molecular Medicine Reports

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The aim of the present study was to determine the effects of curcumin on the osteoclastogenic potential of peripheral blood mononuclear cells (PBMCs) obtained from patients with rheumatoid arthritis (RA), and to investigate the underlying molecular mechanisms. PBMCs from patients with RA (n=12) and healthy controls (n=10) were cultured to assess osteoclastogenic potential. The number of tartrate-resistant acid phosphatase-positive osteoclasts differentiated from PBMCs isolated from patients with RA was significantly increased compared with that of the healthy controls. In addition, the osteoclast number in patients with RA was correlated with the clinical indicators, Sharp score (r=0.810; P=0.001) and lumbar T-score (r=−0.685; P=0.014). Furthermore, the resorption area was increased in the RA group compared with the healthy controls. The mRNA and protein expression levels in PBMC-derived osteoclasts treated with curcumin were measured by reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. Curcumin inhibited the osteoclastogenic potential of PBMCs, potentially by suppressing activation of extracellular signal-regulated kinases 1 and 2, p38 and c-Jun N-terminal kinase, and inhibiting receptor activator of nuclear factor κB (RANK), c-Fos and nuclear factor of activated T cells (NFATc1) expression. The results of the present study demonstrated that curcumin may inhibit the osteoclastogenic potential of PBMCs from patients with RA through the suppression of the mitogen-activated protein kinase/RANK/c-Fos/NFATc1 signaling pathways, and that curcumin may be a potential novel therapeutic agent for the treatment of bone deterioration in inflammatory diseases such as RA.

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Section: Introductionmentioning

confidence: 99%

Curcumin inhibits osteoclastogenic potential in PBMCs from rheumatoid arthritis patients via the suppression of MAPK/RANK/c-Fos/NFATc1 signaling pathways

Shang

Zhao

Dong

et al. 2016

Molecular Medicine Reports

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“…Previous research has confirmed that osteoblast-associated synthesis and secretion of receptor activator of nuclear factor κB ligand (RANKL) and osteoclast-associated RANK are essential in osteoclastogenesis and that RANK binds to RANKL on monocytes, initiating differentiation of osteoclasts [17][18][19]. During this process, an essential transcription factor, nuclear factor kappa B (NF-κB), is activated by the binding of RANKL and RANK via Tumor Necrosis Factor Receptor-associated Factor 6 (TRAF6) and then transported into the nucleus, where it combines with c-Fos, another transcription factor, to activate nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1) to induce osteoclastogenesis [20][21][22][23].…”

Section: Introductionmentioning

confidence: 99%

Curcumin Inhibits Polyethylene-Induced Osteolysis via Repressing NF-κB Signaling Pathway Activation

An¹,

Han²,

Hu³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Aseptic loosening is a common reason for failed artificial hip replacement after total hip arthroplasty. Aseptic loosening is mostly the result of wear debris that causes osteolysis and weakens the structures that support the prosthesis. Wear debris plays a crucial role in osteolysis during the loosening process, and polyethylene (PE) particles are found as wear debris more frequently than any other type of particle. In the absence of effective therapeutic agents, osteolysis has been hard to treat. Previous studies have demonstrated that curcumin influences signalosome-associated kinases and the proteasome-ubiquitin system during osteoclastogenesis. The aims of this study were to explore the anti-osteolysis effect of curcumin and if possible to identify the signaling pathway involved in a model of PE-induced osteolysis. Methods: Differentiation of osteoclasts was induced in vitro by PE particles in RAW264.7 (monocyte/macrophage) cells and in vivo by calvarial and air pouch models of osteolysis established by PE stimulation in mice. We performed a set of TRAP staining, realtime polymerase chain reaction (PCR), and Western blot experiments to evaluate the anti-osteolytic effect of curcumin by comparing specimens that were exposed and not exposed to curcumin. Results: Curcumin had a promising inhibitory effect on osteolysis induced by wear debris and suppressed the RANK/c-Fos/NFATc1 signaling pathway. Conclusion: Curcumin can prevent PE-induced osteolysis and bone loss. An inhibitory effect on the RANK/c-Fos/NFATc1 signaling pathway may explain the anti-osteolysis activity of curcumin.

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“…Receptor activator of nuclear factor κB ligand (RANKL) is a key factor for osteoclasts formation and differentiation. Celastrol, curcumol, pristimerin, andrographolide, jolkinolide B, triterpenoid saponin W3, icariin, aconine, boldine, curcumin, and triptolide can inhibit RANKL‐induced osteoclastogenesis (Gan et al, ; Kong et al, ; Liu et al, ; Ma et al, ; Nanjundaiah et al, ; Shang et al, ; Tong et al, ; Wei, Ping, You, Qiang, & Tao, ; Yu et al, ; Zeng et al, ; Zhai et al, ; Zhao et al, ). Cathepsin K, an enzyme expressed by osteoclasts, degrades key components of bone and cartilage in RA, whose level is directly up‐regulated by RANKL during osteoclastogenesis (Sun et al, ).…”

Section: The Anti‐ra Activities Of Chemical Constituents From Herbal mentioning

confidence: 99%

Herbal compounds for rheumatoid arthritis: Literatures review and cheminformatics prediction

Zhang

2019

Phytotherapy Research

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Rheumatoid arthritis (RA) is a systemic disease characterized by autoimmunity, joint inflammation, and cartilage destruction, which affects 0.5–1% of the population. Many compounds from herbal medicines show the potentials to treat RA. On this basis, the compounds with good pharmacokinetic behaviors and drug‐likeness properties will be further studied and developed. Therefore, the herbal compounds with anti‐RA activities were reviewed in this paper, and the cheminformatics tools were used to predict their drug‐likeness properties and pharmacokinetic parameters. A total of 90 herbal compounds were analyzed, which were reported to be effective on RA models through anti‐inflammation, chondroprotection, immunoregulation, antiangiogenesis, and antioxidation. Most of the herbal compounds have good drug‐likeness properties. Most of the compounds can be an alternative and valuable source for anti‐RA drug discovery.

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Triterpenoid Saponin W3 from Anemone flaccida Suppresses Osteoclast Differentiation through Inhibiting Activation of MAPKs and NF-κB Pathways

Cited by 27 publications

References 28 publications

Curcumin inhibits osteoclastogenic potential in PBMCs from rheumatoid arthritis patients via the suppression of MAPK/RANK/c-Fos/NFATc1 signaling pathways

Curcumin inhibits osteoclastogenic potential in PBMCs from rheumatoid arthritis patients via the suppression of MAPK/RANK/c-Fos/NFATc1 signaling pathways

Curcumin Inhibits Polyethylene-Induced Osteolysis via Repressing NF-κB Signaling Pathway Activation

Herbal compounds for rheumatoid arthritis: Literatures review and cheminformatics prediction

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