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Sargachromanol G regulates the expression of osteoclastogenic factors in human osteoblast-like MG-63 cells
Ist Teil von
Food and chemical toxicology, 2012-09, Vol.50 (9), p.3273-3279
Ort / Verlag
Oxford: Elsevier Ltd
Erscheinungsjahr
2012
Link zum Volltext
Quelle
Elsevier ScienceDirect Journals Complete
Beschreibungen/Notizen
► SG was isolated and purified from the brown alga Sargassum siliquastrum as a novel anti- osteoclastogenic substance. ► We tested whether SG could inhibit IL-1β-induced osteoclastogenic factors in human osteoblast MG-63 cells. ► We also examined the role of SG on NF-κB and MAPK signaling. ► SG inhibited the production of osteoclastogenic factors and the phosphorylation of MAPK and NF-κB in MG-63 cells. ► SG regulates the expression of osteoclastogenic factors via suppression of NF-κB activation and MAPK phosphorylation.
Bone diseases are characterized by the presence of pro-inflammatory cytokines that regulate bone turnover. The receptor activator of NF-κB ligand (RANKL) is a soluble osteoblast-derived protein that induces bone resorption through osteoclast differentiation and activation. Sargachromanol G (SG) was isolated from the brown algae Sargassum siliquastrum; SG has anti-osteoclastogenic activity, but its mechanism of action and its active components remain largely unknown. In the present study, we investigated the anti-osteoclastogenic effects of SG on the expression of interleukin-1β (IL-1β)-induced osteoclastogenic factors (PGE2, COX-2, IL-6, OPG, and RANKL) in the human osteoblast cell line MG-63. We also examined the role of the nuclear factor-κB (NF-κB) and the mitogen-activated protein kinase (MAPK) signaling pathways in IL-1β-stimulated MG-63 cells. SG dose-dependently inhibited the production of osteoclastogenic factors in MG-63 cells. SG also inhibited phosphorylation of MAPK (ERK1/2, p38, and JNK) and NF-κB (p65, p50, and IκB-α). These results suggest that the anti-osteoporotic effect of SG may be because of the modulation of osteoclastogenic factors via suppression of MAPK and NF-κB activation.