Fig. 5.

Induction of IL-1Ra expression by TLR3 activation is dependent on the NF-κB and PI3K-Akt signaling. Human FLS were pre-treated with BMS-345541 (10 μM), LY294002 (25 μM) or SB415286 (25 μM) for 1 h. Subsequently, the cells were stimulated with poly(I:C) for 30 min and the relative levels of IκBα (a), Akt (f), and GSK3β (k) expression and phosphorylation in the different groups of FLSs were measured by Western blot assays. Human FLS were pre-treated with BMS-345541 (10 μM, b–e), LY294002 (25 μM, g–j) or SB415286 (25 μM, l–o) for 1 h and stimulated by poly(I:C) for 8 h or 24 h. The cell viability was measured by CCK-8 assay. The concentrations of IL-1Ra, IFN-β, and IL-6 in the culture supernatants were determined with ELISA. Results are presented as mean ± SEM (n = 5 per group) from 3 separate experiments. * p < 0.05 versus the group with poly(I:C) and vehicle. IL, interleukin; IL-1Ra, IL-1 receptor antagonist.