Anti-osteoclastogenic Effect and Action Mechanisms of the Chromene Isolated from Brown Seaweed

Abstract

In this present study, we investigated the anti-osteoclastogenic effects of sargachromanol G, a kind of chromene, isolated from Sargassum silquastrum on the expressin of IL-1β-induced osteoclastogenic factors (RANKL, IL-6, PGE2, and COX-2) in human osteoblast MG-63 cells, as well as LPS or RANKL-induced pro-inflammatory factors and osteoclastogenic factor [nitric oxide (NO), cytokines (TNF-α, IL-1β, and IL-6), TRAP, CTR, TRAF6, Cath-K, and MMP-9] in murine macrophage RAW 264.7 cells. We also examined the role of nuclear factor- κB (NF-κB) and mitogen activated protein kinase (MAPK) signaling induced by IL-1β in MG-63 and LPS or RANKL in RAW 264.7 cells. Sargachromanol G dose-dependently inhibited the production of osteoclastogenic factors in MG-63 and RAW 264.7 cells. Sargachromanol G also inhibited phosphorylation of NF-κB (IκB- α, p65, and p50) and MAPK (ERK1/2, JNK, and p38). These results suggest that the anti-osteoclastogenic activity of sargachromanol G may result from modulation of osteoclastogenic factors and cytokines via suppression of phosphorylated MAPK and NF-κB activation. in human osteoblast MG-63 cells, as well as LPS or RANKL-induced pro-inflammatory factors and osteoclastogenic factor [nitric oxide (NO), cytokines (TNF-α, IL-1β, and IL-6), TRAP, CTR, TRAF6, Cath-K, and MMP-9] in murine macrophage RAW 264.7 cells. We also examined the role of nuclear factor- κB (NF-κB) and mitogen activated protein kinase (MAPK) signaling induced by IL-1β in MG-63 and LPS or RANKL in RAW 264.7 cells. Sargachromanol G dose-dependently inhibited the production of osteoclastogenic factors in MG-63 and RAW 264.7 cells. Sargachromanol G also inhibited phosphorylation of NF-κB (IκB- α, p65, and p50) and MAPK (ERK1/2, JNK, and p38). These results suggest that the anti-osteoclastogenic activity of sargachromanol G may result from modulation of osteoclastogenic factors and cytokines via suppression of phosphorylated MAPK and NF-κB activation.