Research Paper Volume 11, Issue 7 pp 2003—2019

Figure 1. Genistein prevents CFTR malfunction induced by P31-43. (A) Representative traces of CFTR-dependent Cl- secretion measured by forskolin (Fsk)-inducible chloride current (Isc (μA/cm2)) in Caco-2 cells mounted in Ussing chambers after 3 h of incubation with P57-68 or P31-43 peptides (20 µg/ml), optionally after pre-treatment (20 min) with genistein (50 µM); quantification of the peak CFTR Inhibitor 172 (CFTRinh172)-sensitive Isc (∆Isc) in Caco-2 cells (n= 3 independent experiments). Means±SD of samples assayed; p***<0.001 P57-68 versus P31-43 challenge, °°°p<0.001 P31-43 versus genistein+P31-43 (ANOVA, Bonferroni post-hoc test). (B) Treatment of Caco-2 cells with P57-68, PGAV or P31-43 (3h) or with P31-43 after pre-treatment (20 min) with Genistein. Assessment of iodide efflux by SPQ fluorescent probe upon stimulation with forskolin (Fsk), expressed as percentage of CFTR function. Means±SD of samples assayed; ***p<0.001 P57-68 or PGAV challenge or untreated cells versus P31-43 challenge, °°p<0.01 P31-43 versus Genistein+P31-43 (ANOVA, Bonferroni post-hoc test).