Fig. 3
Effect of canagliflozin treatment on the phosphorylation of AMPK, ACC, eNOS and Akt. a Representative blots and quantification of phosphorylation of AMPK at the Thr172 activation site normalized to total AMPK expression. b Representative blots and quantification of phosphorylation of ACC at the AMPK specific Ser79 residue normalized to total ACC expression. c Representative blots and quantification of phosphorylation of eNOS at the Ser1177 residue normalized to total eNOS expression. d Representative blots and quantification of phosphorylation of Akt at the Ser473 residue normalized to total Akt expression. The number of rats in each experimental group: sham + vehicle (n = 7); sham + canagliflozin (n = 7); IRI + vehicle (n = 9); IRI + canagliflozin (n = 10). Two-way analysis of variance (ANOVA) P values (with factors: ischemia–reperfusion injury [PIRI] and canagliflozin treatment [PCANA]; and their interaction [Pint]) are depicted under the title of each graph for the given variable. Tukey’s post hoc P values are reported as follows: *P < 0.05 versus sham + vehicle; $P < 0.05 versus IRI + vehicle. ACC acetyl-CoA carboxylase, AMPK adenosine monophosphate (AMP)-activated protein kinase, eNOS endothelial nitric-oxide synthase