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Wogonin inhibits osteoclast formation induced by lipopolysaccharide
Author(s) -
Jang Sungil,
Bak Eun Jung,
Kim Minyoung,
Kim Jin Moon,
Chung WonYoon,
Cha JeongHeon,
Yoo YunJung
Publication year - 2010
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.3013
Subject(s) - wogonin , rankl , downregulation and upregulation , osteoclast , osteoprotegerin , calvaria , bone resorption , chemistry , endocrinology , lipopolysaccharide , medicine , activator (genetics) , receptor , scutellaria baicalensis , biochemistry , in vitro , pathology , alternative medicine , traditional chinese medicine , gene
To evaluate the inhibitory activity of wogonin against lipopolysaccharide (LPS)‐induced bone resorption, we investigated the effect of wogonin on osteoclastogenesis induced by LPS. Wogonin inhibited LPS‐induced osteoclastogenesis in co‐cultures of mouse calvaria‐derived osteoblasts and bone marrow‐derived pre‐osteoclasts. Wogonin also suppressed osteoclastogenesis in LPS‐injected mouse calvaria. In osteoblasts, the upregulation of receptor activator of nuclear factor‐κB (RANKL) expression and the downregulation of osteoprotegerin (OPG) expression by LPS were inhibited by wogonin. Wogonin and NS‐398, a COX‐2 inhibitor, suppressed LPS‐stimulated PGE 2 production in osteoblasts. NS‐398 inhibited the effect of LPS on RANKL and OPG expression in osteoblasts. These results suggest that wogonin acts as an inhibitor of LPS‐induced osteoclastogenesis through downregulation of RANKL and upregulation of OPG expression via blockage of PGE 2 production. Based on these results, wogonin has potential for use as a therapeutic agent in bacteria‐induced bone resorption. Copyright © 2009 John Wiley & Sons, Ltd.