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 PI3K/Akt pathways mediate nesfatin-1-induced stimulation of IL-1β synthesis. (A–C) OASFs were treated with a PI3K inhibitor (Ly2942002) or Akt inhibitor (Akti), or transfected with p85 or Akt 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; p85 and Akt phosphorylation was examined by Western blot. (E–F) Quantitative data for p-p85 and p-Akt expression. *p #p

Figure 3. The PI3K/Akt pathways mediate nesfatin-1-induced stimulation of IL-1β synthesis. (AC) OASFs were treated with a PI3K inhibitor (Ly2942002) or Akt inhibitor (Akti), or transfected with p85 or Akt 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; p85 and Akt phosphorylation was examined by Western blot. (EF) Quantitative data for p-p85 and p-Akt expression. *p < 0.05 compared with the control group; #p < 0.05 compared with the nesfatin-1-treated group.