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. Author manuscript; available in PMC: 2012 Mar 1.
Published in final edited form as: Brain Pathol. 2011 Mar;21(2):140–149. doi: 10.1111/j.1750-3639.2010.00430.x

Figure 5. MB increases proteasome activity.

Figure 5

(A) Representative Western blots of proteins extracted from brains of MB-treated and control 3xTg-AD mice probed with antibodies 6E10, CT20, and β-actin as a loading control. (B) Densitometric analysis of blots (normalized to β-actin) indicates that the steady-state levels of APP and the two major c-terminal fragments (C99 and C83) were not affected by MB treatment. Data obtained from 5 treated and 5 untreated 3xTg-AD mice. (C) Representative Western blots of proteins extracted from brains of MB treated and control 3xTg-AD mice probed with different autophagy markers. (D) Densitometric analysis indicates that MB does not significantly affect the steady-state levels of Beclin-1, ATG-7, or LC3B. Data obtained from 5 treated and 5 untreated 3xTg-AD mice. (E–G) Brain homogenates from MB-treated (n=12) and control (n=6) 3xTg-AD mice were analyzed for proteasome activity. The data show that MB increases the chymotrypsin- and trypsin- like activity, while it has no effect on the peptidylglutamyl-peptide hydrolyzing (PDPH) activity. Data are presented as means ± SEM and analyzed by t-test analysis. Abbreviation: Bec-1: Beclin 1. * indicates p<0.05.