Figure 5
Post-ischemic estradiol treatment restores pGSK3Ser21/9 levels in the cerebral cortex but not the hippocampus. Levels of phosphorylated GSK3 and total β-catenin (a substrate of GSK3) were measured in western blots of homogenates from the ipsilateral cerebral cortex (A, B, C) and hippocampus (D, E, F). The bar graphs show the total GSK3 (A, D), the pGSK3Ser21/9 (B, E), and the total β-catenin (C, F), as well as representative blots. The data represent the mean of three to five independent experiments, using β-tubulin or β-actin as loading controls. In the ipsilateral cortex (B) and hippocampus (E), pMCAO (IV group) significantly reduced the pGSK3Ser21/9 levels and total β-catenin levels 54 h after the onset of ischemia when compared with the SV group. Post-pMCAO estradiol treatment attenuated the decrease in pGSK3Ser21/9 (B) and β-catenin (C) levels in the cerebral cortex, but it had no effect on pGSK3Ser21/9 levels in the hippocampus (E). No changes in total β-catenin levels were observed in the hippocampus in any experimental group (F). Total GSK3 levels increased significantly following estradiol treatment in sham operated animals (SE), both in the cortex (A) and hippocampus (C), as compared with the corresponding control (SV) group. The data are expressed as mean ± SEM: * P ≤ 0.05; n = 6 rats per group. IE, pMCAO-estradiol; IV, pMCAO-vehicle; SE, Sham-estradiol; SV, Sham-vehicle.