Figure 3. The combination of UDCA and dexamethasone increases AE activities in hepatobiliary cells.

Cl^–/HCO₃^– AE activity was determined by microfluorimetry in NHCs (A) and PLC/PRF/5 cells (B) following treatments for 24 hours with either dexamethasone and/or UDCA, GUDCA, TUDCA, CA, or CDCA (100 μM each) or with just vehicle. Treated cells were analyzed for AE activities, both baseline (left) and in the presence of a cAMP-stimulation mixture (right). The AE activity was estimated as the rate of pH_i recovery from propionate-induced intracellular alkalinization. Rates of pH_i change were measured as δpH_i/δt from the tangent to the experimental plot; transmembrane acid fluxes (or equivalent transmembrane base fluxes, J_OH^– [mmol/l/min]) were calculated as β_tot × δpH_i/δt, where β_tot is the total intracellular buffering power in the presence of CO₂/HCO₃^–. Data are mean ± SD; n = 9 each. *P < 0.05, **P < 0.01, ***P < 0.001 versus vehicle control.