Fig. 6

Glycogen mobilization regulates astrocytic A1/A2 paradigm via ROS-mediated NF-κB inhibition and STAT3 activation following MCAO/R. a The protein level of GP was analyzed by immunoblotting in frontal cortex area 1 of the astrocyte-specific GP knockdown (KD-GP) mouse brain (n = 6). The vector represents mice intracerebroventricularly injected with mock vector AAVs. b Left panels: representative images using immunofluorescence staining with antibodies against ALDH1L1 and GP in frontal cortex area 1 of the KD-GP mouse brain (n = 8). Right panels: quantitative analysis of the relative fluorescence intensity of GP. The scale bars represent 20 μm. c Cerebral glycogen level at 12 h following MCAO injury (n = 8). d–h Coronal images of the cerebral ischemic penumbra following immunofluorescence staining with antibodies against phosphorylated GS (p-GS, d), phosphorylated GP (p-GP, e), p-NF-κB p65 (g) and p-STAT3 (h) and an antibody against ALDH1L1 after MCAO/R (n = 8). ROS levels were analyzed using the ROS Detection Assay Kit (f). The scale bars represent 20 μm. i, j Coronal images of the cerebral ischemic penumbra following immunofluorescence staining with antibodies against C3 (i) and S100A10 (j) and an antibody against ALDH1L1 after MCAO/R (n = 8). The scale bars represent 20 μm. **P < 0.01, ***P < 0.001. One-way ANOVA followed by LSD post hoc analysis for c–j. One-way ANOVA followed by Dunnett T3 post hoc analysis for a, b