Osteoclastogenic effect of marine algae in human osteoblast-like MG-63 cells

Abstract

Useful secondary metabolites are obtained from marine algae, various species of which are found in Jeju Island, Korea. We aimed to screen marine algae products for their ability to suppress osteoclastogenic factors. Sargachromanol G (SG) which isolated from marine algae 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.ich isolated from marine algae 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.