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. 2022 Jan 10;8:12. doi: 10.1038/s41420-021-00801-9

Fig. 6. Inhibition of AMPK activation eliminates the protective effect of canagliflozin against cisplatin-induced AKI in mice.

Fig. 6

C57BL/6 mice were administered with canagliflozin (CANA) (10 mg/kg) or vehicle orally and intraperitoneally injected with compound C (Comp. C) (5 mg/kg) or saline for five consecutive days, and intraperitoneal injection of cisplatin (20 mg/kg) or saline was done on the 5th day of the treatment. Mice were euthanized at 72 h after cisplatin injection to collect blood samples for measurements of blood urea nitrogen and serum creatinine and kidney tissues for histology. A Representative images of kidney H–E staining (scale bar = 100 μm). B Blood urea nitrogen. C Serum creatinine. D Tubular injury score. Data are expressed as mean ± SD (N = 5–6). Differences between groups were evaluated using one-way ANOVA followed by Bonferroni’s multiple comparison test. ***P < 0.001. NS, not significant. E Representative images of TUNEL staining (scale bar = 60 μm). F Quantification of TUNEL-positive cells in kidney tissues. Data are expressed as mean ± SD (N = 5–6). Differences between groups were evaluated using one-way ANOVA followed by Bonferroni’s multiple comparison test. ***P < 0.001. NS, not significant. G Representative immunoblot analysis. H Densitometric analysis of immunoblots to estimate the relative abundance of cleaved caspase-3 as normalized that of β-actin. Data are expressed as mean ± SD (N = 5). Differences between groups were evaluated using one-way ANOVA followed by Bonferroni’s multiple comparison test. ***P < 0.001. NS, not significant.