Fig. 2 | Scientific Reports

Fig. 2

From: Protein disulfide isomerase integrates toll-like receptor 4 and P2X7 receptor signaling pathways during lipopolysaccharide-induced neuroinflammation

Fig. 2

Effects of P2X7R-mediated NF-κB activation on PDI upregulation in response to LPS. P2X7R deletion cannot affect p65 expression and its S276 phosphorylation under basal condition. LPS augments p65 expression and p65 S276 phosphorylation in P2X7R+/+ mice. P2X7R deletion attenuates these events. SN50 (a NF-κB inhibitor) ameliorates LPS-induced PDI upregulation in P2X7R+/+ and P2X7R−/− mice. (A) Effects of P2X7R deletion on NF-κB activation in response to LPS. Representative Western blot images for p65 expression and p65 S276 phosphorylation (left panel) and quantification of the effects of P2X7R deletion on p65 and p65 S276 densities (right panel) following LPS treatment (#,*p < 0.05 vs. control and P2X7R+/+mice, respectively; Kruskal–Wallis test, n = 7, respectively). (B) Representative photos for p65 S276 phosphorylation in microglia under post-LPS condition. (C) Quantification of the effects of P2X7R deletion on p65 S276 level in microglia under post-LPS condition (*p < 0.05 vs. P2X7R+/+mice, respectively; Mann–Whitney test, n = 7, respectively). (D) Effects of SN50 on PDI expression in response to LPS. Representative Western blot images for PDI expression (left panel) and quantification of the effects of SN50 on PDI density (right panel) under post-LPS condition (#,*p < 0.05 vs. vehicle and P2X7R+/+mice, respectively; Kruskal–Wallis test, n = 7, respectively).

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