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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: A novel role of NLRP3-generated IL-1β in the acute-chronic transition of peripheral lipopolysaccharide-elicited neuroinflammation: implications for sepsis-associated neurodegeneration

Fig. 2

Lacking NLRP3 lessens endotoxemia-elicited increase in IL-1β, but not IL-1α, production. At 9 h after LPS 5 mg/kg or saline ip injection, levels of mature IL-1β (a) and IL-1α (b) were measured in 0.2 mg total protein from brain homogenization of WT and NLRP3−/− mice by ELISA (n = 5–10/group). ***p < 0.001 for (a); NS for (b) between LPS-treated WT and NLRP3−/− groups. Two-way ANOVA followed by Bonferroni post hoc multiple comparison test. c Levels of IL-1β and IL-1α in the supernatant of NLRP3−/− mix-glial cultures at 24 h after vehicle or LPS treatment. Data were from three independent experiments. *p < 0.05, ***p < 0.001, and NS compared to respective vehicle medium group. One-way ANOVA followed by Bonferroni post hoc multiple comparison test. d Mix-glial cultures were treated with 10 ng/ml or 103 ng/ml of LPS or vehicle medium. MCC950 (10 μM) were added to cultures 6 h later. Culture supernatant levels of IL-1β and IL-1α were assessed at 24 h after LPS treatment. Data were from three independent experiments. *p < 0.1, ***p < 0.001, and NS compared with the same dose of LPS treatment group without MCC950. Two-way ANOVA followed by Bonferroni post hoc multiple comparison test

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