Research Paper Volume 13, Issue 18 pp 22490—22501

Nesfatin-1 facilitates IL-1β production in osteoarthritis synovial fibroblasts by suppressing miR-204-5p synthesis through the AP-1 and NF-κB pathways

The AP-1 and NF-κB pathways mediate nesfatin-1-induced stimulation of IL-1β. (A–C) OASFs were treated with an AP-1 inhibitor (tanshinone IIA) or NF-κB inhibitor (PDTC and TPCK), or transfected with c-Jun or p65 siRNAs, then stimulated with nesfatin-1. IL-1β expression was examined by qPCR and ELISA. (D) Cells were incubated with nesfatin-1 for the indicated time intervals; c-Jun and p65 phosphorylation was examined by Western blot. (E–F) Quantitative data for p-c-jun and p-p65 were shown. (G and H) Cells were treated with indicated inhibitors then stimulated with nesfatin-1, and AP-1 and NF-κB luciferase activity was examined. *p #p

Figure 4. The AP-1 and NF-κB pathways mediate nesfatin-1-induced stimulation of IL-1β. (AC) OASFs were treated with an AP-1 inhibitor (tanshinone IIA) or NF-κB inhibitor (PDTC and TPCK), or transfected with c-Jun or p65 siRNAs, then stimulated with nesfatin-1. IL-1β expression was examined by qPCR and ELISA. (D) Cells were incubated with nesfatin-1 for the indicated time intervals; c-Jun and p65 phosphorylation was examined by Western blot. (EF) Quantitative data for p-c-jun and p-p65 were shown. (G and H) Cells were treated with indicated inhibitors then stimulated with nesfatin-1, and AP-1 and NF-κB luciferase activity was examined. *p < 0.05 compared with the control group; #p < 0.05 compared with the nesfatin-1-treated group.