title: Ascorbic acid inhibits osteoclastogenesis of RAW264.7 cells induced by receptor activated nuclear factor kappaB ligand (RANKL) in vitro.
abstract: Ascorbic acid (AA) plays a key role in the regulation of differentiation and activation of osteoclast (OCL). It was reported that AA might induce the formation of OCL in cocultures of mouse bone marrow cells and ST2 cells, but it is not clear whether AA has a direct impact on the OCL precursors. The purpose of this study was to examine the effect of AA on the differentiation of OCL precursor RAW264.7 cells, cultured with receptor-activated nuclear factor kappaB ligand (RANKL). The results showed that AA remarkably inhibited the cell proliferation at a higher concentration and RANKL alone is sufficient for osteoclastogenesis. The expression of carbonic anhydrase (CAII) mRNA and protein, the number of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells (MNCs), and the percentage area of resorption lacunae induced by RANKL were decreased when AA was added to the cultures. The results demonstrate that AA inhibits RANKL-induced differentiation of OCL precursor cells into mature OCL and reduces the formation of bone resorption pits in vitro.
authors.affiliation: Institute of Endocrinology and Metabolism, The Second Xiangya Hospital of Central South University, Changsha, Hunan, PR China.
authors.forename: X H
authors.initials: XH
authors.lastname: Xiao
authors.forename: E Y
authors.initials: EY
authors.lastname: Liao
authors.forename: H D
authors.initials: HD
authors.lastname: Zhou
authors.forename: R C
authors.initials: RC
authors.lastname: Dai
authors.forename: L Q
authors.initials: LQ
authors.lastname: Yuan
authors.forename: X P
authors.initials: XP
authors.lastname: Wu
mesh_terms: D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001205:Ascorbic Acid / Q000494:pharmacology*; D015153:Blotting, Western; D001862:Bone Resorption / Q000473:pathology; D024402:Carbonic Anhydrase II / Q000096:biosynthesis; D002352:Carrier Proteins / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D002454:Cell Differentiation / Q000187:drug effects; D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D007202:Indicators and Reagents; D007527:Isoenzymes / Q000378:metabolism; D008264:Macrophages / Q000187:drug effects*; D008562:Membrane Glycoproteins / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D051379:Mice; D010010:Osteoclasts / Q000187:drug effects*; D053245:RANK Ligand; D012333:RNA, Messenger / Q000096:biosynthesis / Q000302:isolation & purification; D053246:Receptor Activator of Nuclear Factor-kappa B; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000071681:Tartrate-Resistant Acid Phosphatase
chemical_list: D002352:Carrier Proteins; D007202:Indicators and Reagents; D007527:Isoenzymes; D008562:Membrane Glycoproteins; D053245:RANK Ligand; D012333:RNA, Messenger; D053246:Receptor Activator of Nuclear Factor-kappa B; C505687:Tnfrsf11a protein, mouse; C505689:Tnfsf11 protein, mouse; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase; D024402:Carbonic Anhydrase II; D001205:Ascorbic Acid