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. 2020 Dec 24;70(12):2359–2372. doi: 10.1136/gutjnl-2020-321767

Figure 2.

Figure 2

Absence of receptor-interacting protein kinase 3 (RIPK3) ameliorates hepatic inflammation and fibrosis during choline-deficient L-amino acid-defined diet (CDAA) diet-induced experimental non-alcoholic steatohepatitis (NASH). C57BL/6 wild-type (WT) or Ripk3−/− mice were fed a CDAA or an isocaloric control choline-sufficient L-amino acid-defined (CSAA) diet for 32 weeks. (A) Total body weight over time. (B) Liver-to-body weight ratio. (C) Representative images of H&E stained liver sections and immunoperoxidase staining for F4/80. Scale bar=100 µm. (D) Histograms show the quantification of F4/80-positive area (left) and F4/80 mRNA levels (right). (E) Quantitative RT-PCR analysis of Tnf-α, Tlr4, Nlrp3 and Cox-2 in mouse liver. (F) Representative images of Masson’s trichrome stained liver sections. (G) Liver hydroxyproline content. (H) Immunoblotting and densitometry of RIPK3, p-mixed lineage kinase domain-like protein (p-MLKL) and MLKL. Blots of RIPK3 were normalised to endogenous β-actin, whereas p-MLKL was normalised to MLKL. Representative immunoblots are shown. Results are expressed as mean±SEM arbitrary units or fold change of six to seven individual mice. Scale bar=250 µm. §P<0.05 and *p<0.01 from CSAA-fed WT mice; †p<0.05 and ‡p<0.01 from CDAA-fed WT mice.