Fig. 6

Hypoxia-induced decrease of α-ENaC was mediated by the activation of the ERK1/2 and NF-κB signaling pathways. A Immunofluorescence of α-ENaC (green) in AT2 cells cultured in hypoxic condition (8 ml) for 24 h after PD98059 (10 µM) treatment. The nucleus was stained with DAPI (blue). Scale bar = 20 μm. B, C Representative and statistical data of α-ENaC in AT2 cells cultured in hypoxic condition (8 ml) for 24 h after QNZ (NF-κB inhibitor, 100 nM) treatment. n = 4–6. D Representative Isc traces of Control, Hypoxia and Hypoxia + QNZ group in H441 cell monolayers, and amphotericin B (100 µM) was added to the basolateral compartment, followed by 100 µM amiloride applied to the apical side. E Statistic ASI, defined as the difference between the total current and the amiloride-resistant current, n = 4. ***P < 0.001, compared with Control group; ^&P < 0.05, ^&&&P < 0.001, compared with Hypoxia group. One-way ANOVA followed by Bonferroni’s test was used to analyze the difference of the means for significance