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Fig. 8 | Microbiome

Fig. 8

From: Gut microbiota-derived 3-phenylpropionic acid promotes intestinal epithelial barrier function via AhR signaling

Fig. 8

AhR signaling is essential for the 3-phenylpropionic acid-mediated enhancement on the intestinal epithelial barrier function. a Representative western blotting of AhR, Lamin B1, β-actin, and CYP1A1 in the jejunal epithelium of mice from the control (Ctrl) and 3-phenylpropionic acid (3-PPA) groups. b–d Quantitation of AhR levels (b) normalized to Lamin B1 levels. Quantitation of AhR (c) and CYP1A1 (d) levels normalized to β-actin levels. e Representative western blotting of AhR, Lamin B1, β-actin, and CYP1A1 in the jejunal epithelium of mice from the Ctrl and Bacteroides fragilis (BF) groups. f–h Quantitation of AhR levels (f) normalized to Lamin B1 levels. Quantitation of AhR (g) and CYP1A1 (h) levels normalized to β-actin levels. i, j Levels of IL-22 in the jejunal epithelium of mice. k–m Activities of serum diamine oxidase (k) and the levels of endotoxin (l) and D-lactic acid (m), respectively (SR1 StemRegenin 1). n Plasma FD4 levels. o Lactulose/mannitol ratio. p Representative western blotting of ZO-1, E-cadherin, Connexin 43, and β-tubulin in jejunal epithelium of mice. q–s Quantitation of the ZO-1 (q), E-cadherin (r), and Connexin 43 (s) levels normalized to β-tubulin levels. The data are presented as the mean ± SEM and evaluated by Student’s t-test in b–d (n = 3), f–h (n = 3), i (n = 5), and j (n = 10). The data are presented as the mean ± SEM and evaluated by one-way ANOVA with adjustment for multiple comparisons in k–o (n = 8) and q–s (n = 3). **p < 0.01, *p < 0.05; ns not significant

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