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. 2016 Mar 17;14:77. doi: 10.1186/s12967-016-0833-9

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© Li et al. 2016

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 6 — Regulation of COX2 and PGE2 expression is dependent on p38/c-fos and JNK/c-Jun activities. a Effects of IL-17A and MAPK inhibitors on IL-17A induced c-Jun and c-Fos translocation. Nucleoprotein was isolated from NP cells treated with SB203580 (10 or 20 μM), or SP600125 (10 or 20 μM) for 30 min prior to IL-17A (100 ng/ml) induction for 24 h. Afterward, western blot analysis was performed using specific antibodies against c-Jun and c-Fos. Expression of lamin B1 was examined as a reference. The upper panel suggested that the JNK inhibitor SP600125 effectively inhibited IL-17A-induced c-Jun translocation, while the lower panel showed that the p38 inhibitor SB203580 significantly inhibited IL-17A-induced c-Fos translocation. b Pretreatment with combination of SB203580 (10 or 20 μM) and SP600125 (10 or 20 μM) for 30 min prior to IL-17A induction for 24 h in NP cells significantly declined the expression of COX2 and PGE2 (*P < 0.01, vs. control; ^#P < 0.001, vs. IL-17-only treatment). c IL-17A-stimulated COX2 and PGE2 expression depends on AP-1 activation. Pretreatment with curcumin (30 μM) for 30 min prior to IL-17A (100 ng/ml) induction for 24 h in NP cells significantly reduced the expression of COX2 and PGE2 compared with IL-17A-only treatment. (*P < 0.01, vs. control; ^#P < 0.001, vs. IL-17-only treatment)