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. 2019 Mar 11;9:4034. doi: 10.1038/s41598-019-40619-1

Figure 3.

Figure 3

NLRP3 deficiency attenuates the effect of LPS + Aβ on glycolysis and PFKFB3. BMDMs from WT and NLRP3−/− mice were primed with LPS (100 ng/ml) for 3 h, and incubated with Aβ (10 µM) for 24 h. Cell supernatants were collected for analysis by ELISA. LPS + Aβ induced IL-1β production in BMDMs from WT mice (a; ***p < 0.001; WT Con vs WT LPS + Aβ, n = 8 mice/group). IL-1β production, in response to LPS + Aβ, was decreased in BMDMs from NLRP3−/−, compared with WT, mice (a; ###p < 0.001; WT LPS + Aβ vs NLRP3−/− LPS + Aβ, n = 8 mice/group). Metabolic analysis was carried out using the SeaHorse Extracellular Flux (XF24) Analyser. The effect of LPS + Aβ on ECAR and basal glycolysis was decreased in BMDMs from NLRP3−/− mice (b,c; #p < 0.05; WT LPS + Aβ vs NLRP3−/− LPS + Aβ, n = 8–16 mice/group). No change in glycolytic capacity was observed (d). LPS + Aβ increased PFKFB3 in BMDMs from WT mice (e; ***p < 0.001; Con vs LPS + Aβ, n = 4 mice/group). PFKFB3 was decreased in NLRP3−/− BMDMs compared with WT as demonstrated by the representative blot and the mean densitometric data (e; #p < 0.05; WT LPS + Aβ vs NLRP3−/− LPS + Aβ) (Original blot presentation Supplementary Fig. 4). Data are expressed as the mean ± S.E.M. and analysed using a two-way ANOVA and Bonferroni post hoc test.