Fig. 9

Knockdown of S100A9 significantly reduced TLR4/NF-κB and TLR4/p38 signalling pathway activating and decreasing inflammation and apoptosis-related protein expression in EAC mice (n = 6). GSEA analysis showing that TLR4/MyD88, NF-κB, and p38 signalling are activated in IC/BPS patients and EAC mice. (B-C) Knockdown of S100A9 significantly reduced TLR4/NF-κB and TLR4/p38 signalling pathway protein expression in EAC mice. (D-E) Knockdown of S100A9 significantly reduced the expression of bladder inflammation-related proteins (IL-6, IL-1β and TNF-α) in EAC mice. (F) GSEA analysis showing that apoptosis signalling is activated in IC/BPS patients and EAC mice. (G-H) Knockdown of S100A9 expression significantly reduced the expression of bladder apoptosis-related proteins (Bax, caspase-3, caspase-8, and caspase-1) and improved the expression of epithelial damage marker proteins (UPK3A and UPK2) in EAC mice. NS indicates no difference; *p < 0.05, **p < 0.01, ***p < 0.001