{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T05:10:11Z","timestamp":1790917811844,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2011,12,29]],"date-time":"2011-12-29T00:00:00Z","timestamp":1325116800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatism"],"published-print":{"date-parts":[[2012,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Accelerated severe lupus nephritis (ASLN), with an acute onset of severe clinical manifestations and histopathologic renal lesions, may represent transformation of mild LN to a severe form of glomerulonephritis. Abnormal activation of T and B cells and\/or oxidative stress may play a major role in the pathogenesis of ASLN. This study tested the hypothesis that antroquinonol, a purified compound and major effective component of <jats:italic>Antrodia camphorata<\/jats:italic> with antiinflammatory and antioxidant activities, might prevent the transformation of mild LN into higher\u2010grade (severe) nephritis in a murine lupus model.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Experimental ASLN was induced in (NZB \u00d7 NZW)F<jats:sub>1<\/jats:sub> mice by twice weekly intraperitoneal injections of <jats:italic>Salmonella<\/jats:italic>\u2010type lipopolysaccharide (LPS). Starting 2 days after the first dose of LPS, mice were treated daily with antroquinonol, administered by gavage, for different durations up to 5 weeks.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Antroquinonol administration significantly ameliorated the proteinuria, hematuria, impairment of renal function, and development of severe renal lesions, especially cellular crescent formation, neutrophil infiltration, fibrinoid necrosis, and T cell proliferation in the glomerulus, as well as periglomerular interstitial inflammation. Mechanistic analyses revealed that antroquinonol 1) inhibited T cell activation\/proliferation, but enhanced Treg cell suppression and reduced renal production of interleukin\u201018 (IL\u201018); 2) inhibited production of reactive oxygen species and nitric oxide, but increased activation of Nrf2 in the kidney; and 3) suppressed renal inflammation via blocking of NF\u2010\u03baB activation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Antroquinonol may have therapeutic potential for the early treatment of ASLN via its differential regulation of T cell function and lowering of IL\u201018 production, but also via the promotion of Nrf2 activation.<\/jats:p><\/jats:sec>","DOI":"10.1002\/art.33328","type":"journal-article","created":{"date-parts":[[2011,9,8]],"date-time":"2011-09-08T19:58:08Z","timestamp":1315511888000},"page":"232-242","source":"Crossref","is-referenced-by-count":56,"title":["Antroquinonol differentially modulates T cell activity and reduces 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