title: Sargachromanol G inhibits osteoclastogenesis by suppressing the activation NF-κB and MAPKs in RANKL-induced RAW 264.7 cells.
abstract: 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.
authors.affiliation: School of Medicine, Jeju National University, Jeju 690-756, Republic of Korea.
authors.forename: Weon-Jong
authors.initials: WJ
authors.lastname: Yoon
authors.forename: Kil-Nam
authors.initials: KN
authors.lastname: Kim
authors.forename: Soo-Jin
authors.initials: SJ
authors.lastname: Heo
authors.forename: Sang-Chul
authors.initials: SC
authors.lastname: Han
authors.forename: Jihyeon
authors.initials: J
authors.lastname: Kim
authors.forename: Yeong-Jong
authors.initials: YJ
authors.lastname: Ko
authors.forename: Hee-Kyoung
authors.initials: HK
authors.lastname: Kang
authors.forename: Eun-Sook
authors.initials: ES
authors.lastname: Yoo
mesh_terms: D000135:Acid Phosphatase / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001578:Benzopyrans / Q000494:pharmacology*; D056657:Cathepsin K / Q000235:genetics / Q000378:metabolism; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D015870:Gene Expression / Q000187:drug effects; D020672:I-kappa B Proteins / Q000378:metabolism; D015151:Immunoblotting; D007527:Isoenzymes / Q000235:genetics / Q000378:metabolism; D008264:Macrophages / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000235:genetics / Q000378:metabolism; D051379:Mice; D048055:Mitogen-Activated Protein Kinase 8 / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000378:metabolism*; D010010:Osteoclasts / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D053245:RANK Ligand / Q000494:pharmacology*; D018003:Receptors, Calcitonin / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000071681:Tartrate-Resistant Acid Phosphatase; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D001578:Benzopyrans; D020672:I-kappa B Proteins; D007527:Isoenzymes; D016328:NF-kappa B; C000606205:Nfkbia protein, mouse; D053245:RANK Ligand; D018003:Receptors, Calcitonin; C577249:sargachromanol G; D000072000:NF-KappaB Inhibitor alpha; D048055:Mitogen-Activated Protein Kinase 8; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase; D056657:Cathepsin K; D020780:Matrix Metalloproteinase 9