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 3. Grik1 and Grik3 mediate the KA-induced phosphorylation of NF-κB and the expression of NLRP3, IL-1β, and BDNF. Grik1 and Grik3 siRNAs (200 ng) were transfected to BV2 cells before treatment with KA (10 μM) (N=3). (A) Phosphorylation levels of NF-κB and expression levels of NLRP3, IL-1β, and BDNF were determined by Western blotting in KA and/or Grik1/3 transfected BV2 cells. (B) The optical density of bands in Western blotting was analyzed by ImageJ software **P<0.01; ***P<0.001 vs the control group; #P<0.05; ##P<0.01 vs the KA-only treatment.