Trans-3-indoleacrylic acid ameliorates dextran sulfate sodium-induced colitis by modulating macrophage M1 polarization through the aryl hydrocarbon receptor pathway

Figure 3 Trans-3-indoleacrylic acid activates aryl hydrocarbon receptor signaling and suppresses M1 macrophage polarization in vivo. A-C: Concentration of iNOS, IL-1β, and IL-6 in colonic tissues; D-F: Relative mRNA expression of Nos2, Il1b, and Il6 in colonic tissues; G: Representative flow cytometry plots of macrophages from the colon lamina propria. Cells were pre-gated on the CD11b⁺ population. The upper right quadrant (Q2) indicates F4/80⁺CD86⁺ macrophages (M1 macrophages); H: Quantitative analysis of the percentage of F4/80⁺CD86⁺ macrophages among CD11b⁺ cells; I-K: Representative immunoblots and the relative protein expression of AHR and CYP1A1 in colonic tissues; L-O: Relative mRNA expression of Ahr, Cyp1a1, Cyp1b1, and Il22 in colonic tissues. 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 < 0.01, ^bP < 0.001, ^cP < 0.0001. DSS: Dextran sulfate sodium; IDA: Trans-3-indoleacrylic acid; AHR: Aryl hydrocarbon receptor.