title: Aspirin inhibits osteoclastogenesis by suppressing the activation of NF-κB and MAPKs in RANKL-induced RAW264.7 cells.
abstract: Aspirin is a commonly used medicine as an effective antipyretic, analgesic and anti-inflammatory drug. Previous studies have demonstrated its potential effects of anti-postmenopausal osteoporosis, while the molecular mechanisms remain unclear. The effects of aspirin on receptor‑activator of nuclear factor κB (NF‑κB) ligand (RANKL)‑induced osteoclasts were investigated in RAW264.7 cells in the current study. Using tartrate‑resistant acid phosphatase (TRAP) staining, it was observed that aspirin inhibited the differentiation of RANKL‑induced RAW264.7 cells. The mRNA expression of osteoclastic marker genes, including cathepsin K, TRAP, matrix metalloproteinase 9 and calcitonin receptor, were suppressed by aspirin as identified using reverse transcription‑quantitative polymerase chain reaction analysis. The immunofluorescence assay indicated that aspirin markedly inhibited NF‑κB p65 translocation to the nucleus in RANKL‑induced RAW264.7 cells. In addition, aspirin also suppressed the phosphorylation of mitogen‑activated protein kinases (MAPKs), observed by western blot analysis. Taken together, these data identified that aspirin inhibits osteoclastogenesis by suppressing the activation of NF‑κB and MAPKs in RANKL‑induced RAW264.7 cells, implying that aspirin may possess therapeutic potential for use in the prevention and treatment of osteoporosis.
authors.affiliation: Department of Orthopedic Surgery, Institute of Orthopedics, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 830054, P.R. China.
authors.forename: Yan-Ping
authors.initials: YP
authors.lastname: Zeng
authors.affiliation: Department of Orthopedic Surgery, Institute of Orthopedics, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 830054, P.R. China.
authors.forename: Chao
authors.initials: C
authors.lastname: Yang
authors.affiliation: Department of Orthopedic Surgery, Institute of Orthopedics, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 830054, P.R. China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Li
authors.affiliation: Department of Orthopedic Surgery, Institute of Orthopedics, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 830054, P.R. China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Fan
authors.affiliation: Department of Orthopedic Surgery, Institute of Orthopedics, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 830054, P.R. China.
authors.forename: Hong-Jun
authors.initials: HJ
authors.lastname: Yang
authors.affiliation: Department of Orthopedic Surgery, Institute of Orthopedics, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 830054, P.R. China.
authors.forename: Bin
authors.initials: B
authors.lastname: Liu
authors.affiliation: Department of Orthopedic Surgery, Institute of Orthopedics, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 830054, P.R. China.
authors.forename: Hong-Xun
authors.initials: HX
authors.lastname: Sang
mesh_terms: D000818:Animals; D001241:Aspirin / Q000494:pharmacology*; D056657:Cathepsin K / Q000235:genetics; D002454:Cell Differentiation; D015536:Down-Regulation; D020780:Matrix Metalloproteinase 9 / Q000235:genetics; D051379:Mice; D020928:Mitogen-Activated Protein Kinases / Q000187:drug effects* / Q000378:metabolism*; D016328:NF-kappa B / Q000187:drug effects*; D010010:Osteoclasts / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D010012:Osteogenesis / Q000187:drug effects* / Q000502:physiology; D010766:Phosphorylation; D053245:RANK Ligand; D000067996:RAW 264.7 Cells; D018003:Receptors, Calcitonin / Q000235:genetics; D015398:Signal Transduction
chemical_list: D016328:NF-kappa B; D053245:RANK Ligand; D018003:Receptors, Calcitonin; C505689:Tnfsf11 protein, mouse; D020928:Mitogen-Activated Protein Kinases; D056657:Cathepsin K; D020780:Matrix Metalloproteinase 9; D001241:Aspirin