Fig. 3From: Deficiency of the microglial Hv1 proton channel attenuates neuronal pyroptosis and inhibits inflammatory reaction after spinal cord injuryHv1 deficiency reduces activation of the NLRP3 inflammasome after SCI. a–c Representative confocal images showing the NLRP3 inflammasome markers (green) NLRP3 (a), Caspase-1 (b), and ASC (c), as well as the neuronal marker, NeuN (red; scale bar, 50 μm). d–f Quantification of the fraction (%) of d NLRP3-positive neurons (NLRP3+NeuN+ cells/NeuN+ cells × 100), (e) Caspase-1-positive neurons (Caspase-1+NeuN+ cells/NeuN+ cells × 100) and f ASC-positive neurons (ASC+ NeuN+ cells/NeuN+ cells × 100). g Western blotting showing NLRP3, caspase-1 p20, ASC, and IL-18 protein levels. h–k Quantification of Western-blot results for NLRP3 (H), caspase-1 p20 (i), ASC (j), and IL-18 (k) normalized to β-actin. l The expression of IL-18 mRNA via real-time PCR. Data are represented as the mean ± SEM (n = 5 for each treatment; #p < 0.05 ##p < 0.01, SCI vs. sham treatment; *p < 0.05 **p < 0.01, KO SCI vs. WT SCI)Back to article page