Fig. 2: The GPR35 antagonist ML145 inhibits CEC response to BFT in HT29/c1 cells.

HT29/c1 cells were treated for 1 h (a) and 3 h (b) with BFT and increasing concentrations of the GPR35 antagonist ML145 (N = 3). Treatment with ML145 significantly inhibited changes in HT29/c1 cell morphology (two-way ANOVA P = 0.023 and P = 0.015, 1h (a) and 3 h (b), respectively) compared to the positive control (BFT without antagonist—dotted lines). Treatment with 2 and 20 µM of ML145 inhibited BFT morphological changes at 1h and 20 µM ML145 at 3 h (Dunnet’s multiple comparison test *P < 0.05, **P < 0.01, ***P < 0.001). c BFT treatment significantly enhanced the release of E-cadherin into the culture supernatant (P < 0.001). E-cadherin release was significantly inhibited by ML145 (N = 3, P < 0.01). d BFT treatment significantly enhanced IL-8 secretion into the culture supernatant (P < 0.01). IL-8 secretion was significantly inhibited by ML145 (N = 3, P < 0.05; two-way ANOVA with Bonferroni post test in c and d).