Sargachromanol G inhibits osteoclastogenesis by suppressing the activation NF-κB and MAPKs in RANKL-induced RAW 264.7 cells

•We study the anti-ostoclastogenesis effect of SG in RANKL-activated RAW 264.7 cells.•SG inhibits osteoclastogenesis from macrophages in vitro.•SG also reduced the RANKL-induced expression of osteoclastic marker genes.•Moreover, SG attenuated RANKL-induced MAPKs and NF-κB activation. Inflammatory cy...

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Veröffentlicht in:Biochemical and biophysical research communications 2013-05, Vol.434 (4), p.892-897
Hauptverfasser: Yoon, Weon-Jong, Kim, Kil-Nam, Heo, Soo-Jin, Han, Sang-Chul, Kim, Jihyeon, Ko, Yeong-Jong, Kang, Hee-Kyoung, Yoo, Eun-Sook
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container_issue 4
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container_title Biochemical and biophysical research communications
container_volume 434
creator Yoon, Weon-Jong
Kim, Kil-Nam
Heo, Soo-Jin
Han, Sang-Chul
Kim, Jihyeon
Ko, Yeong-Jong
Kang, Hee-Kyoung
Yoo, Eun-Sook
description •We study the anti-ostoclastogenesis effect of SG in RANKL-activated RAW 264.7 cells.•SG inhibits osteoclastogenesis from macrophages in vitro.•SG also reduced the RANKL-induced expression of osteoclastic marker genes.•Moreover, SG attenuated RANKL-induced MAPKs and NF-κB activation. Inflammatory cytokines play a major role in osteoclastogenesis, leading to the bone resorption that is frequently associated with osteoporosis. Sargachromanol G (SG), isolated from the brown alga Sargassum siliquastrum, inhibits the production of inflammatory cytokines. In the present study, we determined the effect of SG on receptor activator of NF-κB ligand (RANKL)-induced osteoclast formation. SG inhibited RANKL-induced osteoclast differentiation from RAW264.7 cells without signs of cytotoxicity. Additionally, the expression of osteoclastic marker genes, such as tartrate-resistant acid phosphatase (TRAP), cathepsin K (CTSK), matrix metalloproteinase 9 (MMP9), and calcitonin receptor (CTR), was strongly inhibited. SG inhibited RANKL-induced activation of NF-κB by suppressing RANKL-mediated IκB-α degradation. Furthermore, SG inhibited RANKL-induced phosphorylation of mitogen activated protein kinases (p38, JNK, and ERK). This study identified SG as an inhibitor for osteoclast formation and provided evidence that natural compounds, such as SG, are an alternative medicines for preventing and treating osteolysis.
doi_str_mv 10.1016/j.bbrc.2013.04.046
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Inflammatory cytokines play a major role in osteoclastogenesis, leading to the bone resorption that is frequently associated with osteoporosis. Sargachromanol G (SG), isolated from the brown alga Sargassum siliquastrum, inhibits the production of inflammatory cytokines. In the present study, we determined the effect of SG on receptor activator of NF-κB ligand (RANKL)-induced osteoclast formation. SG inhibited RANKL-induced osteoclast differentiation from RAW264.7 cells without signs of cytotoxicity. Additionally, the expression of osteoclastic marker genes, such as tartrate-resistant acid phosphatase (TRAP), cathepsin K (CTSK), matrix metalloproteinase 9 (MMP9), and calcitonin receptor (CTR), was strongly inhibited. SG inhibited RANKL-induced activation of NF-κB by suppressing RANKL-mediated IκB-α degradation. Furthermore, SG inhibited RANKL-induced phosphorylation of mitogen activated protein kinases (p38, JNK, and ERK). This study identified SG as an inhibitor for osteoclast formation and provided evidence that natural compounds, such as SG, are an alternative medicines for preventing and treating osteolysis.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2013.04.046</identifier><identifier>PMID: 23611776</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Acid Phosphatase - genetics ; Acid Phosphatase - metabolism ; Animals ; Benzopyrans - pharmacology ; Cathepsin K - genetics ; Cathepsin K - metabolism ; Cell Line ; Cell Survival - drug effects ; Dose-Response Relationship, Drug ; Gene Expression - drug effects ; I-kappa B Proteins - metabolism ; Immunoblotting ; Isoenzymes - genetics ; Isoenzymes - metabolism ; Macrophages - cytology ; Macrophages - drug effects ; Macrophages - metabolism ; MAPK ; Matrix Metalloproteinase 9 - genetics ; Matrix Metalloproteinase 9 - metabolism ; Mice ; Mitogen-Activated Protein Kinase 8 - metabolism ; Mitogen-Activated Protein Kinases - metabolism ; NF-kappa B - metabolism ; NF-KappaB Inhibitor alpha ; NF-κB ; Osteoclastogenesis ; Osteoclastogenic marker gene ; Osteoclasts - cytology ; Osteoclasts - drug effects ; Osteoclasts - metabolism ; p38 Mitogen-Activated Protein Kinases - metabolism ; Phosphorylation - drug effects ; RANK Ligand - pharmacology ; RANKL ; Receptors, Calcitonin - genetics ; Receptors, Calcitonin - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Sagachromanol G (SG) ; Sargassum siliquastrum ; Tartrate-Resistant Acid Phosphatase</subject><ispartof>Biochemical and biophysical research communications, 2013-05, Vol.434 (4), p.892-897</ispartof><rights>2013 Elsevier Inc.</rights><rights>Copyright © 2013 Elsevier Inc. 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Inflammatory cytokines play a major role in osteoclastogenesis, leading to the bone resorption that is frequently associated with osteoporosis. Sargachromanol G (SG), isolated from the brown alga Sargassum siliquastrum, inhibits the production of inflammatory cytokines. In the present study, we determined the effect of SG on receptor activator of NF-κB ligand (RANKL)-induced osteoclast formation. SG inhibited RANKL-induced osteoclast differentiation from RAW264.7 cells without signs of cytotoxicity. Additionally, the expression of osteoclastic marker genes, such as tartrate-resistant acid phosphatase (TRAP), cathepsin K (CTSK), matrix metalloproteinase 9 (MMP9), and calcitonin receptor (CTR), was strongly inhibited. SG inhibited RANKL-induced activation of NF-κB by suppressing RANKL-mediated IκB-α degradation. Furthermore, SG inhibited RANKL-induced phosphorylation of mitogen activated protein kinases (p38, JNK, and ERK). 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Kim, Kil-Nam ; Heo, Soo-Jin ; Han, Sang-Chul ; Kim, Jihyeon ; Ko, Yeong-Jong ; Kang, Hee-Kyoung ; Yoo, Eun-Sook</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c389t-c9a3b2822c4ff51036ca504bb6c2e559a582152ed61a19e545b9cb5772e927e43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Acid Phosphatase - genetics</topic><topic>Acid Phosphatase - metabolism</topic><topic>Animals</topic><topic>Benzopyrans - pharmacology</topic><topic>Cathepsin K - genetics</topic><topic>Cathepsin K - metabolism</topic><topic>Cell Line</topic><topic>Cell Survival - drug effects</topic><topic>Dose-Response Relationship, Drug</topic><topic>Gene Expression - drug effects</topic><topic>I-kappa B Proteins - metabolism</topic><topic>Immunoblotting</topic><topic>Isoenzymes - genetics</topic><topic>Isoenzymes - metabolism</topic><topic>Macrophages - cytology</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>MAPK</topic><topic>Matrix Metalloproteinase 9 - genetics</topic><topic>Matrix Metalloproteinase 9 - metabolism</topic><topic>Mice</topic><topic>Mitogen-Activated Protein Kinase 8 - metabolism</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>NF-KappaB Inhibitor alpha</topic><topic>NF-κB</topic><topic>Osteoclastogenesis</topic><topic>Osteoclastogenic marker gene</topic><topic>Osteoclasts - cytology</topic><topic>Osteoclasts - drug effects</topic><topic>Osteoclasts - metabolism</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Phosphorylation - drug effects</topic><topic>RANK Ligand - pharmacology</topic><topic>RANKL</topic><topic>Receptors, Calcitonin - genetics</topic><topic>Receptors, Calcitonin - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Sagachromanol G (SG)</topic><topic>Sargassum siliquastrum</topic><topic>Tartrate-Resistant Acid Phosphatase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yoon, Weon-Jong</creatorcontrib><creatorcontrib>Kim, Kil-Nam</creatorcontrib><creatorcontrib>Heo, Soo-Jin</creatorcontrib><creatorcontrib>Han, Sang-Chul</creatorcontrib><creatorcontrib>Kim, Jihyeon</creatorcontrib><creatorcontrib>Ko, Yeong-Jong</creatorcontrib><creatorcontrib>Kang, Hee-Kyoung</creatorcontrib><creatorcontrib>Yoo, Eun-Sook</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Calcium &amp; 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Inflammatory cytokines play a major role in osteoclastogenesis, leading to the bone resorption that is frequently associated with osteoporosis. Sargachromanol G (SG), isolated from the brown alga Sargassum siliquastrum, inhibits the production of inflammatory cytokines. In the present study, we determined the effect of SG on receptor activator of NF-κB ligand (RANKL)-induced osteoclast formation. SG inhibited RANKL-induced osteoclast differentiation from RAW264.7 cells without signs of cytotoxicity. Additionally, the expression of osteoclastic marker genes, such as tartrate-resistant acid phosphatase (TRAP), cathepsin K (CTSK), matrix metalloproteinase 9 (MMP9), and calcitonin receptor (CTR), was strongly inhibited. SG inhibited RANKL-induced activation of NF-κB by suppressing RANKL-mediated IκB-α degradation. Furthermore, SG inhibited RANKL-induced phosphorylation of mitogen activated protein kinases (p38, JNK, and ERK). This study identified SG as an inhibitor for osteoclast formation and provided evidence that natural compounds, such as SG, are an alternative medicines for preventing and treating osteolysis.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>23611776</pmid><doi>10.1016/j.bbrc.2013.04.046</doi><tpages>6</tpages></addata></record>
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subjects Acid Phosphatase - genetics
Acid Phosphatase - metabolism
Animals
Benzopyrans - pharmacology
Cathepsin K - genetics
Cathepsin K - metabolism
Cell Line
Cell Survival - drug effects
Dose-Response Relationship, Drug
Gene Expression - drug effects
I-kappa B Proteins - metabolism
Immunoblotting
Isoenzymes - genetics
Isoenzymes - metabolism
Macrophages - cytology
Macrophages - drug effects
Macrophages - metabolism
MAPK
Matrix Metalloproteinase 9 - genetics
Matrix Metalloproteinase 9 - metabolism
Mice
Mitogen-Activated Protein Kinase 8 - metabolism
Mitogen-Activated Protein Kinases - metabolism
NF-kappa B - metabolism
NF-KappaB Inhibitor alpha
NF-κB
Osteoclastogenesis
Osteoclastogenic marker gene
Osteoclasts - cytology
Osteoclasts - drug effects
Osteoclasts - metabolism
p38 Mitogen-Activated Protein Kinases - metabolism
Phosphorylation - drug effects
RANK Ligand - pharmacology
RANKL
Receptors, Calcitonin - genetics
Receptors, Calcitonin - metabolism
Reverse Transcriptase Polymerase Chain Reaction
Sagachromanol G (SG)
Sargassum siliquastrum
Tartrate-Resistant Acid Phosphatase
title Sargachromanol G inhibits osteoclastogenesis by suppressing the activation NF-κB and MAPKs in RANKL-induced RAW 264.7 cells
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