Fig. 7

TRPV4 activation promotes cell death in enteric glial cells (EGCs) via caspase-3 activation, while its inhibition reduces toxin-induced effects. Fluorescence intensity of cleaved caspase-3 was measured in EGCs after 18 h of incubation with GSK1016790A (TRPV4 agonist), TcdA (50 ng/mL), TcdB (1 ng/mL), RN-1734 (TRPV4 antagonist), or their combinations. TRPV4 activation significantly increased caspase-3 cleavage, while its inhibition by RN-1734 reduced the effect induced by both TcdA and TcdB. Data are presented as mean ± SEM (n = 5). Statistical significance was determined using one-way ANOVA and Tukey tests. **p < 0.001, ***p < 0.0001. EGCs following 18 h of incubation with either TcdA (50ng/mL), TcdB (1ng/mL), only EGCs with only DMEM (control group), GSK 1,016,790 A (50nM/mL); RN -1734 alone (100µM), RN-1734 plus TcdA or RN-1734 plus TcdB