Figure 8
CFTR inhibition abolishes inhibitory effect of STS on CSE-induced release in IL-6 and IL-8, but increases CSE-induced activation in ERK/NF-κB pathway. 16HBE cells were treated with 2% CSE for 48 h with 2 h of STS (10 μg/ml) pre-incubation. In order to inhibit CFTR function, cells were treated with CFTR specific inhibitor CFTR-Inh172 (10 μM) 1 h prior to STS treatment. (A) cells were treated with CFTR-Inh172 (0–50 μM) for 48 hours and cell viability was measured by CCK8 assay. (B) IL-6 and IL-8 expression in cell culture medium was measured. (C) The levels of phosphorylated ERK1/2 in cytosol protein were determined with ERK1/2 as internal control (n = 3). The level of p65/NF-κB in nuclear extraction was determined with histone H3 as internal control (n = 6). Full-length blots are presented in supplementary Figure 3. *P < 0.05 and **P < 0.01, CFTR, cystic fibrosis transmembrane conductance regulator; CSE, cigarette smoke extract; CS, cigarette smoke; STS, Sodium tanshinone IIA sulfonate.
