{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,27]],"date-time":"2026-04-27T22:45:01Z","timestamp":1777329901782,"version":"3.51.4"},"reference-count":45,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2018,10,14]],"date-time":"2018-10-14T00:00:00Z","timestamp":1539475200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2019,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Wear particle\u2013induced bone resorption leads to prosthesis loosening, which is a major complication associated with total joint arthroplasty. Although the exact mechanism remains unclear, wear particle\u2013induced extensive osteoclastogenesis plays a critical role in this process. Thus, a potential treatment of prosthetic loosening is focused on suppressing extensive osteoclast formation and bone resorption, which prevents wear particle\u2013induced osteolysis. Arctigenin isolated from <jats:italic>Arctium lappa<\/jats:italic> has numerous beneficial pharmacologic effects, including anti\u2010inflammatory, antiviral, and anticancer activities. Here, we explored the potential impact of arctigenin on titanium (Ti) particle\u2013induced osteolysis in vivo. Our data showed that arctigenin significantly suppressed Ti particle\u2013induced osteolysis and prevented bone destruction compared with Ti group. In addition, the number of osteoclasts reduced after treatment with arctigenin in vivo, indicating osteoclastogenesis might be inhibited by arctigenin. Next, bone marrow\u2013derived macrophages were used to examine osteoclast differentiation, bone resorption, and activation of osteoclast\u2010related signaling pathways. The results showed that arctigenin inhibited RANKL\u2010induced osteoclastogenesis without any cytotoxicity and suppressed osteoclastic marker genes expression and hydroxyapatite resorption activity in a dose\u2010dependent manner. Additionally, arctigenin suppressed receptor activator of nuclear factor \u03ba\u0392 (NF\u2010\u03baB) ligand\u2013induced NF\u2010\u03baB activation, concomitant with retarded I\u03baB\u0251 degradation and inhibition of p65 nuclear translocation, leading to impaired osteoclastogenesis. Collectively, our results suggest that arctigenin is a promising candidate for the treatment of osteoclast\u2010related osteolytic diseases caused by excessive osteoclast formation.<\/jats:p>","DOI":"10.1002\/jcb.27815","type":"journal-article","created":{"date-parts":[[2018,10,14]],"date-time":"2018-10-14T12:45:03Z","timestamp":1539521103000},"page":"5367-5376","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Arctigenin inhibits RANKL\u2010induced osteoclastogenesis and hydroxyapatite resorption in vitro and prevents titanium particle\u2013induced bone loss in vivo"],"prefix":"10.1002","volume":"120","author":[{"given":"Gejin","family":"Wei","sequence":"first","affiliation":[{"name":"Guangxi Medical University Postdoctoral Research Station, Guangxi Medical University Guangxi China"},{"name":"Department of Orthopedics, Hospital of PLA Guangxi 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