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Fig. 2 | Molecular Medicine

Fig. 2

From: Extracorporeal shockwave against inflammation mediated by GPR120 receptor in cyclophosphamide-induced rat cystitis model

Fig. 2

Effects of extracorporeal shock wave treatment (ESWT) and GPR120 agonists on cyclophosphamide (CYP)-stimulated inflammatory response in urothelial RT4 cells. a-e Protein expressions of pro-inflammatory (i.e., TAK1, NF-κB and NLRP3) and anti-inflammatory (i.e., GPR120) markers in CYP-treated RT4 cells at 24 h with and without prior ESWT. f-j 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 agonists (i.e., GW9508 and DHA) compared to those elicited through ESWT. 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; p < 0.05, ††p < 0.01 vs. control; Significance of differences determined by one-way ANOVA followed by Bonferroni’s post-hoc comparisons tests

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