Fig. 6From: TGF-β is elevated in hyperuricemic individuals and mediates urate-induced hyperinflammatory phenotype in human mononuclear cellsBlocking TGF-β signalling pathway partly reverses urate priming effects. Adherent monocytes isolated from healthy volunteers (An = 10; B-C n = 6) were treated with dose-ranging concentrations of urate (50 mg/dL) in the presence or absence of a TGF-β inhibitor for 24 h after which cells were washed and stimulated with LPS (10 ng/mL) for 24 h. IL-1β and IL-Ra were measured in the supernatant after 48 h culture. TGF-β inhibitors: a blocking antibody against TGF-β receptor II with mouse IgG1 as the isotype control (10 μg/mL), SB-505124 (5 μM) and 5Z-7-oxozeaenol (100nM) both with DMSO as solvent control. Wilcoxon signed rank test was applied to compare means. *p < 0.05Back to article page