Fig. 3

Effect of extracorporeal shock wave treatment (ESWT) and GPR120 antagonist on cyclophosphamide (CYP)-stimulated inflammatory response in urothelial RT4 cells. a-e Protein expressions of active pro-inflammatory markers (i.e., p-TAK1 and p-NF-κB) in CYP-stimulated RT4 cells at 4 h with and without prior treatment with GPR120 antagonist (i.e., AH7614) compared to those induced through ESWT. f-h Immunoblotting of RT4 cells treated with GPR120-specific or control (si-cntl) siRNA for 48 h showing that exposure to GPR120-specific siRNA reduced endogenous GPR120 mRNA and protein expression by approximately 50%. i-n Knockdown of GPR120 significantly impaired the ability of ESWT to reduce p-TAK1 and p-NF-κB. β-actin used as internal control for immunoblotting. Values expressed as the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01 vs. CYP/siGPR120; ^†p < 0.05, ^††p < 0.01 vs. control; ^#p < 0.05, vs. CYP + ESWT; ns, non-significance. Significance of differences determined by one-way ANOVA followed by Bonferroni’s post-hoc comparisons tests