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. 2020 Aug 21;12:262. doi: 10.3389/fnagi.2020.00262

Figure 1.

Figure 1

α-Lipoic acid (LA) improved glucose metabolism deficiency in P301S mice. (A) Representative western blots showed the expression levels of glucose transporter 1 (GLUT1), GLUT3, GLUT4, hexokinase-1 (HK-1), and HK2. (B–F) Quantified results of GLUT1, GLUT3, GLUT4, HK1, and HK2 levels between wild type (WT) and P301S mice. β-actin served as an internal loading control. (G) HK activity between WT and P301S mice. (H–L) Quantified results of the levels of GLUT1, GLUT3, GLUT4, HK-1, and HK2 among vehicle, LA 3 mg/kg, and 10 mg/kg groups. β-actin served as an internal loading control. (M) HK activity among vehicles, LA 3 mg/kg, and 10 mg/kg groups. (N–Q) Representative western blots and quantified results of the levels of heme oxygenase-1 (HO-1), vascular endothelial growth factor (VEGF), and proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). β-actin served as an internal loading control. (R–U) mRNA level of GLUT1, GLUT3, GLUT4, and VEGF. Values are represented as the means ± SEM (n = 7). *p < 0.05, **p < 0.01.