Abstract
Epigallocatechin gallate (EGCG), a major polyphenol in green tea, possesses antioxidant properties and regulates various cell functions. Here, we examined the function of EGCG in inflammatory bone resorption. In calvarial organ cultures, lipopolysaccharide (LPS)-induced bone resorption was clearly suppressed by EGCG. In osteoblasts, EGCG suppressed the LPS-induced expression of COX-2 and mPGES-1 mRNAs, as well as prostaglandin E2 production, and also suppressed RANKL expression, which is essential for osteoclast differentiation. LPS-induced bone resorption of mandibular alveolar bones was attenuated by EGCG in vitro, and the loss of mouse alveolar bone mass was inhibited by the catechin in vivo.
Highlights
In bone tissues, bone mass is regulated by bone resorption and bone formation, and bone resorption is elicited by osteoclasts differentiated from the macrophage lineage cells
Epigallocatechin gallate (EGCG) is a major component of the green tea catechins, and has been reported to show the strongest effects among the different catechins on various cell functions, and to exhibit anti-oxidant and anti-tumor activity [8,9]
We found that EGCG acts on osteoblasts to suppress the LPS-induced prostaglandin E2 (PGE2) production by inhibiting the expression of COX-2, membrane-bound PGE synthase (mPGES)-1 and mPGES-2
Summary
Bone mass is regulated by bone resorption and bone formation, and bone resorption is elicited by osteoclasts differentiated from the macrophage lineage cells. We have reported that the bone resorption associated with inflammation was attenuated in mPGES-1-deficient mice (mPges1À/À) due to the lack of PGE production by osteoblasts [7]. Catechin is reported to enhance alkaline phosphatase activity in osteoblasts and osteogenic differentiation of mesenchymal stem cells [11,12], and EGCG inhibits osteoclastic differentiation from macrophage [13], but the effects of EGCG on inflammatory bone resorption are not known. We examined the influence of EGCG on the calvarial bone resorption induced by LPS, and on the COX-2- and mPGES-1-dependent PGE synthesis in mouse osteoblasts. EGCG inhibited LPS-induced osteoclastic bone resorption by suppressing the PGE2 production by osteoblasts in vitro, and attenuated the inflammatory bone loss of the mouse mandibular alveolar bone in vivo
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