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

Figure 3.

Figure 3

Absence of receptor-interacting protein kinase 3 (RIPK3) ameliorates disease severity induced by long-term choline-deficient L-amino acid (CDAA) feeding. C57BL/6 wild-type (WT) or Ripk3−/− mice were fed a CDAA or an isocaloric control choline-sufficient L-amino acid (CSAA) diet for 66 weeks. (A) Liver-to-body weight ratio. (B) Representative images of H&E stained liver sections and immunoperoxidase staining for F4/80. Scale bar=250 µm. (C) Histograms show the quantification of F4/80-positive area (left) and F4/80 mRNA levels (right). (D) Quantitative RT-PCR analysis of Tnf-α, Tlr4, Nlrp3 and Cox-2 in mouse liver. (E) Representative images of Masson’s trichrome stained liver sections. Scale bar=250 µm. (F) Representative macroscopic pictures of livers. The scale bar represents 0.5 cm; arrowhead depicts preneoplastic nodules. (G) Representative immunoperoxidase staining for Ki67. Histogram show the quantification of Ki67-positive cells in percentage. Scale bar=100 µm. (H) Immunoblotting and densitometry of RIPK3, 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. §P<0.05 and *p<0.01 from CSAA-fed WT mice; †p<0.05 from CDAA-fed WT mice.