Cromene regulates the expression of osteoclastogenic factors in human osteoblast-like MG-63 cells

Abstract

Bone diseases are characterized by the presence of pro-inflammatory cytokines that regulate bone turnover. The receptor activatorof NF-kB ligand (RANKL) is a soluble osteoblast-derived protein that induces bone resorption through osteoclast differentiation and activation. Sagachromanol G (SG) was isolated from the brown algae Sagassum 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-1b(IL-1b)-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-kB (NF-kB) and the mitogen-activated protein kinase (MAPK) signaling pathways in IL-1b-stimulated MG-63 cells. SG dose-depenently inhibited the production of osteoclastogenic factors in MG-63 cells. SG also inhibited phosphorylation of MAPK (ERK 1/2, p38, and JNK) and NF-kB (p65, p50, and IkB-a). 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-kB activation. differentiation and activation. Sagachromanol G (SG) was isolated from the brown algae Sagassum 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-1b(IL-1b)-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-kB (NF-kB) and the mitogen-activated protein kinase (MAPK) signaling pathways in IL-1b-stimulated MG-63 cells. SG dose-depenently inhibited the production of osteoclastogenic factors in MG-63 cells. SG also inhibited phosphorylation of MAPK (ERK 1/2, p38, and JNK) and NF-kB (p65, p50, and IkB-a). 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-kB activation.