Figure 6.

AE ameliorates autophagy impairment in APP-PSEN1 mice by activating ADRB2 mediates MTOR autophagy signaling. (A and B) the levels of ATG5, ATG7, LC3-II:I and SQSTM1/p62 in the hippocampus were detected using western blotting and quantitatively analyzed. (C) Representative confocal images of LC3 and 4G8 immunofluorescence colabeling. (D) quantification of the number of LC3-positive cells near Aβ plaques. (E) electron microscopy analysis of autophagosomes. Arrows indicate the autophagosomes (scale bar: 0.5 μm). (F) quantification of autophagosomes. (G) Representative pictures of autophagic flux and (H) quantification of LC3 puncta in (G). (I-J) the levels of MTOR, p-MTOR, PRKAA and p-PRKAA/AMPK in the hippocampus were detected using western blotting and quantitatively analyzed. (K and L) VMA21 protein levels between the AE and propranolol-inhibited groups. n = 6 mice per group. (K and M) Vma21 protein levels after silencing Adrb2 in BV2 cells. n = 6. *P < 0.05; **P < 0.01; ***P < 0.001 and ****P < 0.0001. The data are presented as the means ± SEMs. Student’s t tests were used to analyze the data in (A-F and L), one-way ANOVA followed by Bonferroni’s post hoc test was used to analyze the data in (H and M) and two-way ANOVA followed by Bonferroni’s post hoc test was used to analyze the data in (J).