{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,23]],"date-time":"2026-01-23T23:20:10Z","timestamp":1769210410238,"version":"3.49.0"},"reference-count":41,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2012,6,15]],"date-time":"2012-06-15T00:00:00Z","timestamp":1339718400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2012,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Interleukin\u20106 (IL\u20106) is a pleiotropic cytokine secreted by macrophages and others and it has been proven to be a potential therapeutic target of RA. Norisoboldine (NOR) is the main isoquinoline alkaloid constituent in the dry roots of <jats:italic>Lindera aggregata<\/jats:italic> (Sims) Kosterm. (<jats:italic>L. strychnifolia<\/jats:italic> Vill.), which has long been used in traditional Chinese medicine for treating RA and other diseases. Our previous studies indicated that NOR was able to attenuate inflammation and joint destruction in collagen II\u2010induced arthritis of mice. To further recognize the anti\u2010rheumatoid potentials of NOR, the present study addressed whether and how NOR interfered with IL\u20106 production from fibroblast\u2010like synoviocytes (FLS), key effector cells in the development and progression of RA. FLS, obtained from the synovial tissues of rats with adjuvant arthritis, showed incremental release of IL\u20106 after stimulated with IL\u20101\u03b2 in vitro. NOR (10, 30, and 60\u2009\u00b5M) could reduce the production of IL\u20106 in a concentration\u2010dependent manner. It also down\u2010regulated the phosphorylations of mitogen\u2010activated protein kinases (MAPKs), protein kinase C (PKC), and transcriptional factor nuclear factor\u2010\u03baB (NF\u2010\u03baB)\u2010p65 (ser 276) as well as cAMP response element\u2010binding protein (CREB) in FLS. By using specific inhibitors, PKC was shown to be the upstream protein of MAPKs, and p38 MAPK was at the upstream of CREB. It was concluded that preventing IL\u20106 release from FLS might be an important mechanism for NOR displaying anti\u2010RA property, and the action of NOR was relative to inhibition of PKC\/MAPKs\/p65\/CREB pathways. J. Cell. Biochem. 113: 2785\u20132795, 2012. \u00a9 2012 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jcb.24156","type":"journal-article","created":{"date-parts":[[2012,4,3]],"date-time":"2012-04-03T13:36:45Z","timestamp":1333460205000},"page":"2785-2795","source":"Crossref","is-referenced-by-count":35,"title":["Norisoboldine inhibits the production of interleukin\u20106 in fibroblast\u2010like synoviocytes from adjuvant arthritis rats through PKC\/MAPK\/NF\u2010\u03baB\u2010p65\/CREB 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