Figure 1 | Scientific Reports

Figure 1

From: Urolithin A-mediated augmentation of intestinal barrier function through elevated secretory mucin synthesis

Figure 1

Results of the administration of Uro A to the 6-week mice. (a) Control group: The MUC2 immunostaining of wild-type (C57BL/6) mice colon. The MUC2-positive mucus layer is dark brown. (b) Uro A group: The MUC2 immunostaining of the colon in wild-type (C57BL/6) mice treated with Uro A (100 mg/kg). The MUC2-positive mucus layer is stained dark brown (marked by "↔"). (c) The thickness of the MUC2-positive mucus layer in the Uro A group is significantly greater than that in the control group (n = 6, control group; 6.47 ± 2.03 µm, Uro A group; 11.52 ± 1.93 µm, p < 0.01, Wilcoxon rank sum test). (d) As evaluated by ELISA, the MUC2 protein level in the colonic mucosal epithelium is significantly higher in the Uro A group than in the control group (n = 6, control group; 100.0 ± 35.8, Uro A group; 142.0 ± 33.6, p = 0.041, Wilcoxon rank sum test). (e) Uro A treatment does not increase MUC2 protein levels in the colonic epithelium of Nrf2-deficient mice (n = 6, control group; 100.0 ± 48.0, Uro A group; 75.6 ± 36.8, p = 0.309, Wilcoxon rank sum test). (f) The MUC2 protein level in mice treated intraperitoneally with an AhR antagonist did not increase in the colonic epithelium after Uro A treatment (n = 6, control group; 100.0 ± 20.3, Uro A group; 82.8 ± 26.1, p = 0.222, Wilcoxon rank sum test). Uro A, urolithin A; MUC2, mucin 2; ELISA, enzyme-linked immunosorbent assay; Nrf2, NF-E2-related factor 2.

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