Fig. 4.

The effect of postconditioning on phosphorylated and total protein levels of phosphoinositide-dependent protein kinase-1 (PDK1), phosphatase and tensin homologue deleted on chromosome 10 (PTEN), and glycogen synthase kinase 3β (GSK 3β) after stroke. Representative protein bands of phosphorylated and total PDK1, PTEN, and GSK 3β are shown along with their corresponding mean optical densities (bar graphs). For brevity, β-actin bands were omitted. Levels of phosphorylated proteins are shown in a, b, and c for PDK1, PTEN, and GSK 3β, respectively. Protein levels of phosphorylated-PDK1 (P-PDK1), phosphorylated-PTEN (P-PTEN), and phosphorylated glycogen synthase kinase 3β (P-GSK3β) decreased after ischemia. (a) The P-PDK1 levels were reduced at 24 h in postconditioned control ischemic brains in the penumbra; they were reduced at 24 h postischemia with or without postconditioning in the ischemic core.*p < 0.05, **p < 0.01 versus sham. (b) Although postconditioning slightly attenuated the reduction in P-PTEN levels at 1, 5, and 24 h in the penumbra, no significant difference was detected between postconditioning and control ischemia. *p < 0.05, **p < 0.01, and ***p < 0.001 versus sham. (c) P-GSK3β levels were transiently increased at 1 h in only the penumbra, and then reduced at 5 and 24 h in both the penumbra and core in rats with control ischemia; they were reduced in rats with postconditioning in both the penumbra and core postischemia. *p < 0.05, **p < 0.01,***p < 0.001 versus sham; #p < 0.05 versus 1 h/con in the penumbra; ##p < 0.01 versus 1 h/con in the core, n = 4–5/group.