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. 2025 Feb 26;21(5):2313–2329. doi: 10.7150/ijbs.105667

Figure 4.

Figure 4

rIPC reverses the upregulation of NOX4 in AKI. (A) Representative heatmap of differentially expressed genes in the kidneys of CP-AKI mice (n=3). (B) Comparable analysis between cisplatin and cisplatin + rIPC group using Gene Set Enrichment Analysis (GSEA). (C) NOX4 expression assessed by Western blot in cisplatin, LPS and IRI-induced AKI. (D) Representative image of immunochemistry staining of NOX4 in kidney tissue sections (200x, scale bar = 50μm). (E) rIPC reverses the upregulation of NOX4 assessed by RT-qPCR, western blot and quantified by densitometry in mice kidney (n=6). (F) Representative image of immunofluorescence staining of NOX4 in CP-AKI mouse kidney (200x, scale bar = 10μm). (G) rIPC reverses the upregulation of NOX4 assessed by RT-qPCR, western blot and quantified by densitometry in TCMK-1 (n=3). (H) NOX4 inhibitor GKT137831 improved the pathological injury and tubular damage score in CP-induced AKI mice under hematoxylin and eosin (H&E) staining (200x, scale bar = 50μm; 400x, scale bar = 20 μm). Data are presented as mean ± SD, n = 6. rIPC: remote ischemic preconditioning, CP: cisplatin, CCCP: carbonyl cyanide 3-chlorophenylhydrazone, LPS: lipopolysaccharides, IRI: ischemia/reperfusion injury. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001, #p<0.05, ##p<0.01, ###p<0.001, ####p<0.0001.