Figure 7. Effects of diclofenac on CaCC, IRC and Ca²⁺-activated basolateral K⁺ channel.

(A) Inhibition of CaCC-mediated Cl⁻ transport by diclofenac. (left) Representative tracing of CaCC-mediated apical Cl⁻ current with basolateral membrane permeabilization. CFTR_inh-172 (5 µM) and ATP (100 µM) were added into apical solutions before addition of diclofenac into both apical and basolateral solutions (n = 5). (right) Diclofenac had no effect on ATP-induced CaMKII phosphorylation. T84 cells were incubated for 20 min with vehicle (control), ATP (100 µM), or ATP (100 µM) plus diclofenac (20 µM). CaMKII phosphorylation was investigated using immunoblot analysis of phosphorylated CaMKII. Results of band intensity analysis are expressed as relative band intensity. NS, non-statistical difference; *, p<0.05 compared with control (n = 3). (B) Inhibition of IRC-mediated Cl⁻ transport by diclofenac. In this experiment, apical Cl⁻ current analysis was performed. CFTR_inh-172 (5 µM) was added into apical solution before IRC activation by forskolin (20 µM). Diclofanac was added into both apical and basolateral solutions (n = 5). (C) Inhibition of Ca²⁺-activated basolateral K⁺ channel (K_Ca3.1) by diclofenac. In this experiment, basolateral K⁺ current measurements were performed in the presence of BaCl₂ (5 mM) in the apical solution. DMSO (control) or diclofenac was added into both apical and basolateral solutions before activation of K_Ca3.1 by ATP (100 µM) (n = 4–6).