{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T16:06:12Z","timestamp":1787241972465,"version":"build-2736575974"},"reference-count":35,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2017,5,1]],"date-time":"2017-05-01T00:00:00Z","timestamp":1493596800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Periodontology"],"published-print":{"date-parts":[[2017,5]]},"abstract":"<jats:p>\n                    <jats:bold>Background:<\/jats:bold>\n                    Periodontitis is a chronic inflammatory disease initiated by bacteria and their virulence factors. Bortezomib (BTZ) is the first proteasome inhibitor for clinical treatment of malignancies. Its anticancer activity is accompanied by an anti\u2010inflammatory effect. However, there are few reports about its anti\u2010inflammatory effect and underlying mechanism in periodontal disease, especially on human periodontal ligament cells (hPDLCs), which are considered a promising cell\u2010based therapy for treating periodontitis.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Methods:<\/jats:bold>\n                    hPDLCs were treated with lipopolysaccharide (LPS) and pretreated with BTZ. mRNA and protein levels of tumor necrosis factor (TNF)\u2010alpha, interleukin (IL)\u20101\u03b2, IL\u20106, and IL\u20108 were determined. The anti\u2010inflammatory mechanism of BTZ was studied. Further, experimental rat periodontitis was induced with ligature and LPS injection, and simultaneously and locally treated with BTZ (three injections\/week). Four weeks after treatment, microcomputed tomography, immunohistochemical, and histopathologic analyses were performed.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results:<\/jats:bold>\n                    Bortezomib administration at safe concentrations (\u22641 nM) inhibited production of proinflammatory cytokines in LPS\u2010stimulated hPDLCs via nuclear factor (NF)\u2010kappa B, p38\/extracellular signal\u2010regulated kinase, and mitogen\u2010activated protein kinase\/activator protein\u20101 pathways. Moreover, in the LPS and ligature\u2010induced periodontitis rat model, BTZ suppressed expression of TNF\u2010\u03b1, IL\u20101\u03b2, IL\u20106, and IL\u20108, reduced the ratio of receptor activator of NF\u2010\u03baB ligand\/osteoprotegerin, and prevented alveolar bone absorption.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusion:<\/jats:bold>\n                    These findings demonstrate the anti\u2010inflammatory activity of BTZ against periodontal inflammatory response and present BTZ as a promising therapy for periodontal disease.\n                  <\/jats:p>","DOI":"10.1902\/jop.2016.160396","type":"journal-article","created":{"date-parts":[[2016,12,16]],"date-time":"2016-12-16T10:11:22Z","timestamp":1481883082000},"page":"473-483","source":"Crossref","is-referenced-by-count":19,"title":["The Proteasome Inhibitor Bortezomib Inhibits Inflammatory Response of Periodontal Ligament Cells and Ameliorates Experimental 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