peptide protects tMCAo model from neuronal damage. A, schematic timeline of the transient ischemic stroke model and treatment. B, representative images of rat brain sections stained with TTC from rats subjected to tMCAo. TAT-GAPDH2-2-1-1 peptide (40 nmol) was administrated via i.c.v. injection 30 min after the onset of stroke. C, Infarct area of tMCAo rats brain in a series of brain slices according to the Stereotactic Coordinates in TAT-GAPDH2-2-1-1 and TAT only groups. D, neurological score of tMCAo rats in each group. Neurological score was assessed both 2 h and 24 h after reperfusion. ANOVA, followed by post-hoc SNK test (*p<0.05). E, Statistic analysis of the tMCAo infarct volume in each group. The infarct volume of TAT-GAPDH2-2-1-1 group is significantly smaller than that in the TAT only group (172.8±27.93 mm3vs. 296.0±41.11 mm3, n=8 in each group, p<0.05). ANOVA, followed by post-hoc SNK test. F, statistics analysis of tMCAo infarct volume after 1d, 3d and 5d of the stroke onsets (n=8 per group). G, CoIP of GAPDH by p53 from nuclear proteins in rat cortex of sham, TAT-GAPDH2-2-1-1 and tMCAo only groups (n=3 per group). ANOVA, followed by post-hoc SNK test. (two sets of experiments are normalized by the tMCAo only group) H, Western blot analysis of GAPDH nuclear expression in rat cortical tissues from sham, tMCAo, TAT-GAPDH2-2-1-1 (top) and TAT-GAPDH2-2-1-1SCRM (bottom) groups. The experiments were conducted in two sets. The first set of experiments included three groups: sham, TAT-GAPDH2-2-1-1 and the tMCAo. The second set of experiments included two groups: the scrambled peptide and the tMCAo group. The bar graph represents each group normalized with the tMCAo group in the same set of experiments. **Significantly different from sham group (n=3 per group, p<0.01); ##significantly different from tMCAo group (n=3 per group, p<0.01); ANOVA, followed by post-hoc SNK test.