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. 2023 Mar 24;14:1142240. doi: 10.3389/fimmu.2023.1142240

Figure 5.

Figure 5

Inhibition of NK-1R with a pharmacological antagonist attenuated UUO-induced renal fibrosis, inflammation, and apoptosis. (A, B) RT-qPCR (A) and Western blotting (B) showed that the inhibition of NK-1R antagonized the UUO-induced increase in Collagen I, α-SMA, MCP-1, and TNF-α at the mRNA and/or protein levels in renal cortical tissues on day 14 after UUO. For B, representative images (left panels) and quantitative data (right panels) are shown. (C) PAS, Masson’s trichrome, F4/80 immunochemistry staining, and TUNEL analysis displayed that the inhibition of NK-1R impeded renal fibrosis, infiltration of F4/80-positive inflammatory cells, and apoptosis mediated by UUO surgery. Representative images (upper panels) and quantitative data (lower panels) are shown. For (A–C), sham and UUO mice were administered intraperitoneally with vehicle (DMSO) or a specific NK-1R inhibitor (NK-1Ri) SR140333 (1 mg/kg body weight) every day for 14 days. + or −, with (+) or without (−) the indicated treatment. TUNEL-positive cells were counted by fluorescence microscopy in ten randomly selected high-power fields per kidney section. Scale bar, 50 µm. Data are shown as mean ± SEM from groups of six mice. **p < 0.01; ***p < 0.001; ****p < 0.0001.