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. 2022 Mar 7;28(9):918–932. doi: 10.3748/wjg.v28.i9.918

Figure 4.

Figure 4

Cystic fibrosis transmembrane conductance regulator protected the Caco2 cells from hypoxia/reoxygenation-induced apoptosis by PI3K/AKT/NF-κB pathway. A: Representative images of immunofluorescence staining for NF-κB P65 in Caco2 cells after the LV-cystic fibrosis transmembrane conductance regulator (CFTR) transfection (n = 3); B: Representative western blotting and quantification data for PI3K, p-AKTser473, p-AKTThr308, and NF-κB P65 after LV-CFTR transfection, aP < 0.01 and bP < 0.001 vs control (n = 3); C: Cell viability was tested using the CCK8 kit after LV-CFTR transfection and treatment with NF-κB activator Betulinic acid (BA), AKT inhibitor GSK690693 and PI3K inhibitor LY294002, bP < 0.001 vs control (n = 3); D: Representative Western blotting and quantification data for cell apoptotic proteins Bcl-2 and Bax after LV-CFTR transfection and treatment with NF-κB activator BA, AKT inhibitor GSK690693 and PI3K inhibitor LY294002. Data are presented as mean ± SD. bP < 0.001 vs control (n = 3).