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. 2018 Mar 14;9(3):401. doi: 10.1038/s41419-018-0433-0

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — a Inhibitory effects of kaempferol on ex vivo osteoclast formation. The BMMs obtained from CIA + vehicle and CIA + kaempferol mice were analyzed in terms of the osteoclast formation induced by M-CSF or M-CSF + RANKL. TRAP⁺ osteoclasts (≥3 nuclei/TRAP⁺ cell) were counted. Photographs (×100) are representative of TRAP staining obtained from each mouse group (CIA + vehicle, n = 3; CIA + kaempferol, n = 3), and values obtained from the whole well of a 48-well plate are presented as means ± SEM. *p < 0.05. b Inhibitory effects of kaempferol on in vitro osteoclast formation. Naïve murine BMMs were subjected to osteoclast differentiation by combinational stimulation of kaempferol, M-CSF, and RANKL as indicated. TRAP⁺ osteoclasts ( ≥ 3 nuclei/TRAP⁺ cell) were counted. Photographs (×100) are representative of TRAP staining obtained from three independent experiments, and values obtained from the whole well of a 48-well plate are represented as means ± SEM. *p < 0.05; **p < 0.01; ***p < 0.001. c Inhibitory effects of kaempferol on osteoclast-specific genes. Naïve murine BMMs stimulated with M-CSF/RANKL and indicated doses of kaempferol for 4 days, and mRNA levels of indicated osteoclast-specific genes were measured by real-time PCR. Data were obtained from three independent experiments, and values are represented as means ± SEM. **p < 0.01; ***p < 0.001. d Representative photographs of morphological osteoclast analysis. The indicated area shows a multinucleated giant osteoclast cell body after treatment with kaempferol and M-CSF/RANL, as indicated. Scale bars, 40 μm. e Inhibitory effects of kaempferol on osteoclast differentiation. The total nuclear number of multinucleated (≥3 nuclei) giant cells with the phenotypic features of osteoclasts and the number of cells with a single nucleus were counted. Data were obtained from three independent experiments using a four-chamber slide, and values are represented as means ± SEM. *p < 0.05; **p < 0.01; ***p < 0.001. f Schematic of the signaling pathway targeted by kaempferol for the inhibition of osteoclast differentiation. bFGF-FGFR3 interaction transduces activation signaling to RSK2, resulting in hyperplasia by the induction of inflammation, FLS proliferation, and cell migration through NF-κB and AP-1. Eventually, the macrophages in synovium differentiate to bone absorbing osteoclasts. Thus, the dual targeting of kaempferol on both FGFR3 and RSK2 may prevent RA in humans

Fig. 6 — a Inhibitory effects of kaempferol on ex vivo osteoclast formation. The BMMs obtained from CIA + vehicle and CIA + kaempferol mice were analyzed in terms of the osteoclast formation induced by M-CSF or M-CSF + RANKL. TRAP⁺ osteoclasts (≥3 nuclei/TRAP⁺ cell) were counted. Photographs (×100) are representative of TRAP staining obtained from each mouse group (CIA + vehicle, n = 3; CIA + kaempferol, n = 3), and values obtained from the whole well of a 48-well plate are presented as means ± SEM. *p < 0.05. b Inhibitory effects of kaempferol on in vitro osteoclast formation. Naïve murine BMMs were subjected to osteoclast differentiation by combinational stimulation of kaempferol, M-CSF, and RANKL as indicated. TRAP⁺ osteoclasts ( ≥ 3 nuclei/TRAP⁺ cell) were counted. Photographs (×100) are representative of TRAP staining obtained from three independent experiments, and values obtained from the whole well of a 48-well plate are represented as means ± SEM. *p < 0.05; **p < 0.01; ***p < 0.001. c Inhibitory effects of kaempferol on osteoclast-specific genes. Naïve murine BMMs stimulated with M-CSF/RANKL and indicated doses of kaempferol for 4 days, and mRNA levels of indicated osteoclast-specific genes were measured by real-time PCR. Data were obtained from three independent experiments, and values are represented as means ± SEM. **p < 0.01; ***p < 0.001. d Representative photographs of morphological osteoclast analysis. The indicated area shows a multinucleated giant osteoclast cell body after treatment with kaempferol and M-CSF/RANL, as indicated. Scale bars, 40 μm. e Inhibitory effects of kaempferol on osteoclast differentiation. The total nuclear number of multinucleated (≥3 nuclei) giant cells with the phenotypic features of osteoclasts and the number of cells with a single nucleus were counted. Data were obtained from three independent experiments using a four-chamber slide, and values are represented as means ± SEM. *p < 0.05; **p < 0.01; ***p < 0.001. f Schematic of the signaling pathway targeted by kaempferol for the inhibition of osteoclast differentiation. bFGF-FGFR3 interaction transduces activation signaling to RSK2, resulting in hyperplasia by the induction of inflammation, FLS proliferation, and cell migration through NF-κB and AP-1. Eventually, the macrophages in synovium differentiate to bone absorbing osteoclasts. Thus, the dual targeting of kaempferol on both FGFR3 and RSK2 may prevent RA in humans