Fig. 3
From: Poldip2 mediates blood-brain barrier disruption in a model of sepsis-associated encephalopathy
Heterozygous deletion of Poldip2 abrogates LPS-induced NF-κΒ/Cox2 signaling in vivo. Poldip2+/+ and Poldip2+/− mice were treated with LPS (18 mg/kg, IP) or PBS to examine NF-κΒ/Cox2 signaling in vivo. a Immunoblotting for the NF-κΒ subunit p65 and Cox2 was performed on cerebral cortices of Poldip2+/+ and Poldip2+/− mice after 6 h of treatment. β-tubulin was used as a loading control. Representative blots are shown. b p65 expression was quantified by densitometry. The graph depicts p65 expression normalized to β-tubulin. Error bars represent mean ± SEM. Two-way ANOVA *p < 0.05 vs. Poldip2+/+ + PBS, ##p < 0.01 vs. Poldip2+/+ + LPS, n = 6 mice/group. c Cox-2 expression was quantified by densitometry. The graph depicts Cox-2 expression normalized to β-tubulin. Bars represent mean ± SEM. Two-way ANOVA **p < 0.01 vs. Poldip2+/+ + PBS, #p < 0.05 vs. Poldip2+/+ + LPS, n = 6 mice/group. d PGE2 levels in the cerebral cortices of Poldip2+/+ and Poldip2+/− mice were assessed by ELISA after 18 h of LPS or PBS. The graph depicts PGE2 concentrations normalized by total protein concentration. Bars represent mean ± SEM. Two-way ANOVA, ***p < 0.001 vs. Poldip2+/+ + PBS, #p < 0.05 vs. Poldip2+/+ + LPS, n = 4–6 mice/group