Salvianolic Acid B Attenuates Iopromide-Induced Renal Tubular Epithelial Cell Injury by Inhibiting the TLR4/NF-κB/NLRP3 Signaling Pathway

Figure 3

(a) Schematic diagram of the molecular docking between Sal B and target proteins. A, B: conformation of Sal B (green) and target proteins; C, D: the binding sites of Sal B (green) with TLR4 or NLRP3; E, F: schematic diagram of Sal B binding to TLR4 or NLRP3; G, H: the docking amino acid residues of Sal B and TLR4 or NLRP3. Sal B decreased the protein levels of TLR4, NLRP3, ASC, Caspase-1, p-NF-κB, IL-18, IL-1β, and TNF-α. (b) Iopromide treatment caused a significant increase in TLR4, NLRP3, ASC, and Caspase-1. Sal B counteracted the iopromide-induced increase in these protein levels. n = 3. Data are the mean ± SD. vs. control group; ^#, ^## vs. iopromide group. (c) The protein levels of p-NF-κB, IL-18, IL-1β, and TNF-α were significantly increased in iopromide-treated cells. These changes were reduced by 100 μmol/L Sal B n = 3. Data are the mean ± SD. , vs. control group; ^#, ^## vs. iopromide group.

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