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

Fig. 3. Canagliflozin activates AMPK and inhibits mTOR in HK-2 cells and protects HK-2 cells from cisplatin in an AMPK activation-dependent manner.

Fig. 3

HK-2 cells were treated with indicated concentrations of cisplatin and/or canagliflozin (CANA) for 24 h (A–C). A Representative immunoblot analysis. B, C Densitometric analysis of immunoblots to estimate the relative abundance of indicated molecules as normalized that of total AMPK or total mTOR, respectively. Data are expressed as mean ± SD (N = 4). Differences between groups were evaluated one-way ANOVA followed by Bonferroni’s multiple comparison test. *P < 0.05, **P < 0.01, ***P < 0.001, significantly different from the control. HK-2 cells were treated with indicated concentrations of cisplatin, canagliflozin, and/or compound C (Comp. C) for 24 h (D–F). D Cell viability was evaluated by CCK-8 assay. 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. E Representative immunoblot analysis. F 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 < 0.01. NS, not significant.