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

Figure 6 Trans-3-indoleacrylic acid attenuates lipopolysaccharide-stimulated M1 polarization through aryl hydrocarbon receptor signaling in vitro. A: Representative immunoblots of aryl hydrocarbon receptor (AHR) in AHR knockdown THP-1 macrophages; B-D: Concentration of iNOS, IL-1β, and IL-6 in THP-1 macrophage culture supernatants; E-G: Relative mRNA expression of NOS2, IL1B, and IL6 in THP-1 macrophages; H: Representative flow cytometry histograms of the CD80 expression levels in THP-1 macrophages; I: Quantification of FITC-CD80 mean fluorescence intensity; J-L: Representative immunoblots and the relative protein expression of AHR and CYP1A1 in THP-1 macrophages; M-O: Relative mRNA expression of AHR, CYP1A1, CYP1B1, and IL22 in THP-1 macrophages. The data are shown as the mean ± SD (n = 3 cell 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. AHR: Aryl hydrocarbon receptor; NC: Negative control; LPS: Lipopolysaccharide; IDA: Trans-3-indoleacrylic acid; MFI: Mean fluorescence intensity.