Research Paper Volume 11, Issue 11 pp 3795—3810
Kainic acid Induces production and aggregation of amyloid β-protein and memory deficits by activating inflammasomes in NLRP3- and NF-κB-stimulated pathways
Figure 5. IL-1β shows addictive effects whereas BDNF shows antagonistic effects of KA on inducing the expression of BACE1. (A and B) Protein levels of BACE1 in the brains of KA (10 mg/kg)- or Bay11-7082 (1 or 2 mg/kg)+KA-treated APP23 mice (N=6). (C and D) Protein levels of BACE1 in the brains of KA- or IL-1β (1 μg/kg)+KA-treated APP23 mice (N=6). (E and F) Protein levels of BACE1 in the brains of KA- or BDNF (1 μg/kg)+KA-treated APP23 mice (N=6). (G and H) IL-1β and (I and J) BDNF were knocked down in the BV2 cells and the conditional medium was collected for the incubation of N2a cells. Protein levels of BACE1 were determined by Western blotting (N=3). The optical density of bands in Western blotting was analyzed by ImageJ software *P<0.05, **P<0.01, and ***P<0.001 vs the controls; #P<0.05; ##P<0.01 vs the KA group; the significant differences from the respective values were determined by the one-way analysis of variance test.