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The natural flavonoid trifolirhizin (TRI) has anti\u2010inflammatory properties; however, its function in inflammatory bone lysis remains unclear. This study aimed to elucidate the potential regulatory mechanisms of TRI in osteoclasts.Tartrate\u2010resistant acid phosphatase (TRAP) staining, acid secretion assays, podosomal actin belt fluorescence staining, and bone resorption assays were used to investigate the effects of TRI on osteoclast differentiation and bone resorption. A reactive oxygen species (ROS) measurement kit was used to detect the effect of TRI on ROS levels in osteoclasts. The effects of TRI on genes and signaling pathways related to osteoclast differentiation were determined by quantitative polymerase chain reaction (qPCR) and western blotting. A mouse model of lipopolysaccharide\u2010mediated inflammatory osteolysis was established, and the effects of TRI treatment on bone mass were observed using micro\u2010CT and histological examination. Mechanistically, TRI reduced ROS production by inhibiting receptor activator of nuclear factor\u2010\u03baB ligand (RANKL)\u2010induced activation of the nuclear factor\u2010\u03baB (NF\u2010\u03baB) and mitogen\u2010activated protein kinase (MAPK) signaling pathways, and by upregulating the expression levels of the anti\u2010ROS enzymes heme oxygenase\u20101 (HO\u20101) and catalase (CAT), which contributed to the degradation of ROS, ultimately leading to a decrease in osteoclastogenesis. TRI inhibited osteoclast formation and ameliorated lipopolysaccharide (LPS)\u2010mediated inflammatory osteolysis. Thus, TRI may be a candidate agent for anti\u2010inflammatory osteolysis.<\/jats:p>","DOI":"10.1002\/ptr.8299","type":"journal-article","created":{"date-parts":[[2024,8,5]],"date-time":"2024-08-05T02:09:49Z","timestamp":1722823789000},"page":"4650-4666","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Trifolirhizin reduces osteoclast formation and prevents inflammatory osteolysis by inhibiting RANKL\u2010induced activation of NF\u2010\u03baB and MAPK signaling pathways and ROS"],"prefix":"10.1002","volume":"38","author":[{"given":"Jian","family":"Huang","sequence":"first","affiliation":[{"name":"Guangxi Key Laboratory of Regenerative Medicine, Orthopaedic Department The First Affiliated Hospital of Guangxi Medical University  Nanning China"},{"name":"Collaborative Innovation Centre of Regenerative Medicine and Medical BioResource Development and Application Co\u2010constructed by the Province and Ministry, Life 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