{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T11:08:58Z","timestamp":1788520138917,"version":"build-2803163510"},"reference-count":30,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2024,6,27]],"date-time":"2024-06-27T00:00:00Z","timestamp":1719446400000},"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":["Cell Biology International"],"published-print":{"date-parts":[[2024,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>This study explores the potential role and mechanism of Ginsenoside Rb3 (Rb3) in modulating osteoclastogenesis induced by human periodontal ligament fibroblasts (hPLFs) within the periodontitis microenvironment. We investigated the anti\u2010inflammatory effects of Rb3 on hPLFs stimulated with <jats:italic>Porphyromonas gingivalis<\/jats:italic> lipopolysaccharide (<jats:italic>P.g<\/jats:italic>\u2010LPS) utilizing quantitative polymerase chain reaction (qPCR) and enzyme\u2010linked immunosorbent assay techniques. Moreover, the functional role of Rb3 in hPLFs\u2010induced osteoclast formation was assessed by treating human bone marrow\u2010derived macrophages (hBMMs) with conditioned medium from hPLFs, followed by analyses through qPCR, western blot analysis, and staining for tartrate\u2010resistant acid phosphatase (TRAP) and phalloidin. The impact of Rb3 on the activation of the STAT3 signaling pathway was determined via western blot analysis. Results indicated that Rb3 treatment significantly suppressed the upregulation of pro\u2010inflammatory cytokines (TNF\u2010\u03b1, IL\u20101\u03b2, IL\u20106, MCP\u20101, and IL\u201018) at both gene and protein levels in hPLFs induced by <jats:italic>P.g<\/jats:italic>\u2010LPS. Furthermore, conditioned medium from Rb3 plus <jats:italic>P.g<\/jats:italic>\u2010LPS treated hPLFs notably decreased the number of TRAP\u2010positive cells, actin ring formations, and the expression of osteoclast marker genes (including CTSK, NFATC1, and ACP5). Rb3 also inhibited the <jats:italic>P.g<\/jats:italic>\u2010LPS\u2010induced activation of the STAT3 pathway, with the activation of STAT3 partially reversing the effects of Rb3 on inflammation and osteoclast differentiation. Collectively, Rb3 ameliorates inflammation in <jats:italic>P.g<\/jats:italic>\u2010LPS\u2010stimulated hPLFs and reduces hPLFs\u2010induced osteoclastogenesis by inhibiting the STAT3 signaling pathway, suggesting its potential as a therapeutic agent for periodontitis.<\/jats:p>","DOI":"10.1002\/cbin.12201","type":"journal-article","created":{"date-parts":[[2024,6,27]],"date-time":"2024-06-27T10:11:27Z","timestamp":1719483087000},"page":"1343-1353","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Ginsenoside Rb3 alleviates the formation of osteoclasts induced by periodontal ligament fibroblasts in the periodontitis microenvironment through the STAT3 pathway"],"prefix":"10.1002","volume":"48","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-2737-7489","authenticated-orcid":false,"given":"Yuhua","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Stomatology Fujian Medical University Union 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