Figure 6

LCA reduces intestinal inflammation in the early stages of NEC in a PXR-dependent manner. (a) Expression levels of transcripts for IL-6 (i) and TLR4 (ii) in intestinal tissues obtained from WT controls (Ctrl) or WT mice subjected to early stage (day 2) of NEC +/− LCA supplementation. (b) Expression levels of transcripts for (i) IL-6 and (ii) TLR4 in intestinal tissues obtained from PXR^−/− Ctrl or PXR^−/− mice subjected to early stage NEC +/− LCA supplementation. (c) Quantification of NEC severity in WT mice subjected to early stage NEC +/− LCA supplementation. (d) Expression levels of transcripts for (i) IL-6 and (ii) TLR4 in intestinal tissues obtained from WT Ctrl or WT mice subjected to day 4 NEC +/− LCA supplementation. Expression levels were relative to β-actin. *P⩽0.05, **P⩽0.01, ***P⩽0.001 when compared to Ctrl group by Kruskal–Wallis ANOVA with Dunn’s post-test. Results are representative of two to four separate experiments with three (controls) and five to six mice (day 2 NEC) per group in c, and at least four mice per group in (a, b, and d). ANOVA, analysis of variance; LCA, lithocholic acid; LPS, lipopolysaccharide; NEC, necrotizing enterocolitis; PXR, pregnane X receptor.