Figure 5 | Pediatric Research

Figure 5

From: Targeting the PXR–TLR4 signaling pathway to reduce intestinal inflammation in an experimental model of necrotizing enterocolitis

Figure 5

The ability of LCA to diminish LPS-induced production of IL-6 in intestinal tissues is PXR-dependent. (a) Expression levels of LPS-induced transcripts for IL-6 (i) and TNFα (ii) in IEC-6 enterocytes pretreated or not with 100 μM of LCA (24 h) in the absence or presence of PXR siRNA or scrambled siRNA (200 μM). (b) Expression levels of LPS-induced transcripts for IL-6 (i and ii) and TNF-α (iii) in intestinal organoids obtained from WT or PXR−/− mice that were pretreated or not with 100 μM of LCA (16 h). Exposures to LPS were for 2 h at 1 μg/ml (a) or 4 h at 10 μg/ml (b). Results shown are for experiments performed in triplicate. Fold changes were calculated by comparing to untreated cells or organoids and normalized to β-actin. *P0.05, **P0.01, by ANOVA with Tukey’s multiple comparison test (a), or unpaired t-test (b); ANOVA, analysis of variance; LCA, lithocholic acid; LPS, lipopolysaccharide; n.s., not significant; PXR, pregnane X receptor.

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