Fig. 1

Ex-4 ameliorates tau hyperphosphorylation in the T2D mice hippocampus and high-glucose-injured HT22 cells. A Male C57BL/6 mice were divided into three groups. Mice fed a normal diet as the WT group; others establish the HF-diabetic mice model. The HF-diabetic mice which treated daily with exendin-4 (10 µg/kg) for 4 weeks as the Ex-4 group. The phosphorylated tau at Ser199, Ser202, Ser396, and Thr217 sites and total tau in the hippocampus were examined by immunoblotting. B Gray density of A. C Male db/db mice were divided into two groups. One was treated daily with exendin-4 (10 µg/kg) for 4 weeks, and the others were treated with saline, db/m mice as the control. The phosphorylated tau at Ser199, Ser202, Ser396, and Thr217 sites and total tau in the hippocampus were examined by immunoblotting. D Gray density of C. E HT22 cells under the control (CON) or high glucose (50 mM, HG) environment for 48 h, then part of cells in the HG group treated with exendin-4 (10 nM, HG + Ex-4) for 48 h. Immunoblot demonstrates changes in phosphorylated tau at Ser199, Ser202, Ser396, and Thr217 sites and total tau. F Gray density of E. β-actin was used as the internal standard. For A, C, and E, n = 4/group. All results are representative of three independent experiments. Values are presented as mean ± SD. ** P < 0.01, *** P < 0.001, **** P < 0.0001