Research Paper Volume 15, Issue 21 pp 11740—11763

Figure 1. 1,5-AF activates pAMPK, decreases infarct volume, and reduces neurological deficits. Representative TTC-stained cerebral sections from 1,5-AF and control rats (A); infarct volume (white region) was smaller in 1,5-AF rats than in control rats (1,5-AF: n = 6, control: n = 6). Neurological scores (1,5-AF: n = 6, control: n = 6) (B) and mortality rate (1,5-AF: n = 6, control: n = 6) (C) after AIS. Neurological scores were better and mortality rate was lower in 1,5-AF rats than in control rats. Immunoblotting results after AIS (1,5-AF: n = 4, control: n = 4) (D). Semiquantitative analysis of immunoblots revealed that protein levels of pAMPK (E), PGC-1α (F), and BDNF (G) were higher in 1,5-AF rats than in control rats. Photomicrographs of PGC-1α and BDNF immunoreactivities (1,5-AF: n = 6, control: n = 6) (H). PGC-1α (I) and BDNF (J) expression was higher in 1,5-AF rats than in control rats. Data are shown as the mean ± standard error. ^*p < 0.05, ^**p < 0.01, ^***p < 0.001. Scale bar = 50 μm. Abbreviations: 1,5-AF: 1,5-anhydro-D-fructose; AIS: acute ischemic stroke; BDNF: brain-derived neurotrophic factor; pAMPK: phosphorylated 5’-adenosine monophosphate-activated protein kinase; PGC-1α: peroxisome proliferator-activated receptor-γ co-activator-1α; TTC: 2,3,5-triphenyltetrazolium chloride.