Figure 1

PVP-I suppressed LPS plus ATP induced activations of NLRP3 inflammasome response and associated signal molecules in airway epithelial cells (A549 and RPMI2650 cells). Treatment with PVP-I inhibited LPS/ATP-induced activation of NLRP3 inflammasome protein in A549 cells and RPMI2650 cells, as shown in (a) immunoblot and (b) qRT-PCR. Cells were stimulated with LPS and ATP for 24 h, and PVP-I (0.1%) was additionally added to the cells for 1 h (to produce an inflammation environment) after LPS and/or ATP stimulation. (c) and (d) Expression of NF-κB-p65, caspase-1 and IL-1β were also inhibited by PVP-I treatment in airway epithelial cells, as shown by immune blot and qRT-PCR. (e) Cytosolic and nuclear extracts were analyzed by immunoblot with indicated antibodies for NF-κB-p65 and IκB-α. Anti-Lamin B and anti-α-tubulin antibodies were used as loading controls for the nucleus and cytosol, respectively. Statistical significance: *P < 0.05 and **P < 0.01 compared with the control group; ^#P < 0.05, ^##P < 0 .01 and ^###P < 0.01 compared with the LPS/ATP group.