Fig. 1

GSK3β inactivation by SB216763 protects hearts and retains mitoHK-II. a Representative recording of left ventricular (LV) pressure in Langendorff-perfused hearts. The isolated hearts were subjected to I/R in the absence (I/R) or presence of SB216763 (I/R + SB 3 μmol/l). In SB216763-treated hearts, SB216763 was pretreated for 25 min before ischemia, and then hearts were subjected to I/R without SB216763. b Time course of changes in left ventricular developed pressure (LVDP) during I/R in the absence (I/R ○) and presence of SB216763 (I/R + SB ●). The values are mean ± SEM from 6 to 8 experiments. *P < 0.05 vs. I/R by two-way ANOVA followed with Bonferroni’s test. c Western-blot analysis of mitoHK-II in hearts from a, b and non-ischemic control (CTL). Data are presented as fold-increase of mitoHK-II/COXIV ratio from CTL, and values are mean ± SEM from six independent experiments. ^†P < 0.01 by one-way ANOVA followed with Bonferroni’s test. d, e Western-blot analysis of mitoHK-II in permeabilized myocytes. Cells were exposed to GSK3β (GSK; 10 nmol/l), GSK3β plus SB216763 (GSK + SB 3 μmol/l), and DCCD (1 μmol/l) for 1 h, and the mitochondrial fraction was then extracted. Data are presented as fold-increase of mitoHK-II/COXIV from control (CTL) and values are mean ± SEM from seven experiments. ^†P < 0.05 by one-way ANOVA followed by Bonferroni’s test