Figure 3 | Scientific Reports

Figure 3

From: Lack of NLRP3-inflammasome leads to gut-liver axis derangement, gut dysbiosis and a worsened phenotype in a mouse model of NAFLD

Figure 3

Nlrp3−/−-HFHC showed higher hepatic lipid uptake and increased ROS production. HFHC increased PPAR γ1 in a genotype-independent manner, whereas Nlrp3−/−-HFHC mice showed higher expression of PPAR γ2 and its downstream effectors FABP4 and CD36 (a). Gene expression of ACC, FAS and SCD-1 (b). Measurements of plasma indexes of de novo lipogenesis and SCD-1 activity (c–d). Gene expression of PPAR α and of its downstream genes CPT1A and ACOX-1 and expression of the regulator of antioxidant response NRF2 (e). Representative images of liver sections stained with DHE (magnification, 20×) and its morphometric analysis (f). Mean ± SE: çp < 0.05 vs Wt-Chow diet; ççp < 0.01 vs Wt-Chow diet; çççp < 0.001 vs Wt-Chow diet; #p < 0.05 vs Nlrp3−/−-Chow diet; ##p < 0.01 vs Nlrp3−/−-Chow diet; ###p < 0.001 vs Nlrp3−/–Chow diet; ùp < 0.05 vs Wt-HFHC; ùùp < 0.01 vs Wt-HFHC; *p < 0.05; ***p < 0.001.

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