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Thus, searching for natural compounds that may suppress osteoclast formation and\/or function is promising for the treatment of osteoclast\u2010related diseases. Here, we examined changes in osteoclastogenesis and\n LPS<\/jats:styled-content>\n \u2010induced osteolysis in response to andrographolide (\n AP<\/jats:styled-content>\n ), a diterpenoid lactone isolated from the traditional\n C<\/jats:styled-content>\n hinese and\n I<\/jats:styled-content>\n ndian medicinal plant\n \n A<\/jats:styled-content>\n ndrographis paniculata\n <\/jats:italic>\n .\n <\/jats:p>\n <\/jats:sec>\n \n Experimental Approach<\/jats:title>\n \n Effects of\n AP<\/jats:styled-content>\n on osteoclast differentiation and bone resorption were measured\n in vitro<\/jats:italic>\n . Western blots and RT\u2010PCR techniques were used to examine the underlying molecular mechanisms. The bone protective activity of\n AP<\/jats:styled-content>\n \u2005\n in vivo<\/jats:italic>\n was assessed in a mouse model of osteolysis.\n <\/jats:p>\n <\/jats:sec>\n \n Key Results<\/jats:title>\n \n AP<\/jats:styled-content>\n concentration\u2010dependently suppressed\n RANKL<\/jats:styled-content>\n \u2010mediated osteoclast differentiation and bone resorption\n in vitro<\/jats:italic>\n and reduced the expression of osteoclast\u2010specific markers, including tartrate\u2010resistant acid phosphatase, calcitonin receptors and cathepsin\n K<\/jats:styled-content>\n . Further molecular analysis revealed that\n AP<\/jats:styled-content>\n impaired\n RANKL<\/jats:styled-content>\n \u2010induced\n NF<\/jats:styled-content>\n \u2010\n \u03baB<\/jats:styled-content>\n signalling by inhibiting the phosphorylation of TGF\u2010\u03b2\u2010activated kinase 1, suppressing the phosphorylation and degradation of\n I\u03baB\u03b1<\/jats:styled-content>\n , and subsequently preventing the nuclear translocation of the\n NF<\/jats:styled-content>\n \u2010\n \u03baB<\/jats:styled-content>\n p65 subunit.\n AP<\/jats:styled-content>\n also inhibited the\n ERK<\/jats:styled-content>\n \/\n MAPK<\/jats:styled-content>\n signalling pathway without affecting p38 or\n JNK<\/jats:styled-content>\n signalling.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions and Implications<\/jats:title>\n \n AP<\/jats:styled-content>\n suppressed\n RANKL<\/jats:styled-content>\n \u2010induced osteoclastogenesis through attenuating\n NF<\/jats:styled-content>\n \u2010\n \u03baB<\/jats:styled-content>\n and\n ERK<\/jats:styled-content>\n \/\n MAPK<\/jats:styled-content>\n signalling pathways\n in vitro<\/jats:italic>\n , thus preventing bone loss\n in vivo<\/jats:italic>\n . These data indicated that\n AP<\/jats:styled-content>\n is a promising natural compound for the treatment of osteoclast\u2010related bone diseases.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/bph.12463","type":"journal-article","created":{"date-parts":[[2013,10,14]],"date-time":"2013-10-14T07:16:00Z","timestamp":1381734960000},"page":"663-675","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":112,"title":["Andrographolide suppresses\n RANKL<\/scp>\n \u2010induced osteoclastogenesis\n in vitro<\/i>\n and prevents inflammatory bone loss\n in vivo<\/i>"],"prefix":"10.1111","volume":"171","author":[{"given":"Z J","family":"Zhai","sequence":"first","affiliation":[{"name":"Shanghai Key Laboratory of Orthopaedic Implants Department of Orthopaedics Ninth People's Hospital Shanghai Jiao Tong University School of Medicine Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H 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