Fig. 8

AAV2/8-APN^Tri treatment reduces NLRP3-inflammasome activation in the 5xFAD mice. A Iba1 (red) and NLRP3 (green) double-immunofluorescent staining in the hippocampus and cortex of AAV2/8-GFP-treated, and AAV2/8-APN^Tri-treated 5xFAD. (n = 6 mice for each experimental group) (Magnification: 10 × 20; Scale bar: 50μm). B Relative intensity of microglial NLRP3 in the hippocampus and cortex of AAV2/8-GFP-treated, and AAV2/8-APN^Tri-treated 5xFAD. (C) Relative intensity of NLRP3 in the hippocampus and cortex of AAV2/8-GFP-treated, and AAV2/8-APN^Tri-treated 5xFAD. (D) Iba1 (green) and ASC (red) double-immunofluorescent staining in the hippocampus and cortex of AAV2/8-GFP-treated, and AAV2/8-APN^Tri-treated 5xFAD. (n = 6 mice for each experimental group) (Magnification: 10 × 20; Scale bar: 50μm). E Percentage of Iba1 + ASC + cells in the hippocampus and cortex of AAV2/8-GFP-treated, and AAV2/8-APN^Tri-treated 5xFAD. F Relative intensity of microglial ASC in the hippocampus and cortex of AAV2/8-GFP-treated, and AAV2/8-APN^Tri-treated 5xFAD. (G) Western blotting assay of ASC, Pro-caspase-1, and cleaved caspase-1 in the hippocampus of AAV2/8-GFP-treated and AAV2/8-APN^Tri-treated 5xFAD. (n = 5 mice for each experimental group). H Densitometric analysis of ASC, pro-caspase-1, and cleaved caspase 1. (I) ELISA assay of hippocampal IL-1β of AAV2/8-GFP-treated and AAV2/8-APN^Tri-treated 5xFAD. (n = 6 mice for each experimental group). (J) ELISA assay of hippocampal IL-18 of AAV2/8-GFP-treated and AAV2/8-APN^Tri-treated 5xFAD. (n = 5 mice for each experimental group). Data were presented as the mean ± s.e.m. n.s. not significant; *p < 0.05; **p < 0.01; ***p < 0.001. Statistical analyses in (B, C, E, F, G, and H) were performed by unpaired t tests and (I, J) were performed by one-way ANOVA followed with Bonferroni’s post hoc comparison tests.