Copyright: ©Author(s) 2026.
World J Gastroenterol. Dec 14, 2026; 32(46): 123696
Published online Dec 14, 2026. doi: 10.3748/wjg.123696
Published online Dec 14, 2026. doi: 10.3748/wjg.123696
Figure 4 Aryl hydrocarbon receptor inhibition abrogates the protective effects of trans-3-indoleacrylic acid on dextran sulfate sodium-induced colitis.
A: Schematic of the animal experiment; B: Body weight change (%) of mice during dextran sulfate sodium (DSS) treatment; C: Disease activity index score during DSS treatment; D: Representative images of colons from each group; E: Colon length; F: Spleen index; G: Representative images of colonic sections stained with hematoxylin and eosin; H: Histological scores; I: Representative images of colonic sections stained with alcian blue-periodic acid-Schiff; J: Number of goblet cells. The data are shown as the mean ± SD (n = 6 mice per group). Group comparisons were analyzed using one-way ANOVA with Sidak’s multiple comparisons test. aP < 0.05, bP < 0.01, cP < 0.001, dP < 0.0001. In B and C, the P values indicate the differences between groups on day 7. DSS: Dextran sulfate sodium; IDA: Trans-3-indoleacrylic acid; AHRI: Aryl hydrocarbon receptor inhibitor; DAI: Disease activity index; H&E: Hematoxylin and eosin. AB-PAS: Alcian blue-periodic acid-Schiff.
- Citation: Tuo JW, Wu X, Shen ZH, Wang XY. Trans-3-indoleacrylic acid ameliorates dextran sulfate sodium-induced colitis by modulating macrophage M1 polarization through the aryl hydrocarbon receptor pathway. World J Gastroenterol 2026; 32(46): 123696
- URL: https://www.wjgnet.com/1007-9327/full/v32/i46/123696.htm
- DOI: https://dx.doi.org/10.3748/wjg.123696