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. 2018 May 3;9:904. doi: 10.3389/fimmu.2018.00904

Figure 7.

Figure 7

miR-155 antagomir treatment ameliorates dextran sulfate sodium (DSS) colitis pathogenesis and the proposed mechanism. (A–C) WT mice with DSS colitis were administered i.v. antagomir-155 (5 mmol/kg per mouse) or scrambled controls as the schematic protocol indicated, and miR-155 expression level and its functional targets C/EBPβ and SOCS1 were determined by Q-PCR and western blotting respectively. (D,E) The DAI (E) and survival rate (E) of WT mice with DSS colitis that were treated with antagomir-155 or of NC mice were monitored daily till day 15 after DSS challenge. (F) The representative immunofluorescence images (left) and the quantification (right) of M1 and M2 in colon tissues co-stained with macrophage F4/80 (green), iNOS/Arg1 (red), and DAPI (nuclei, blue). (G) The relative expression of M1 genes and M2 genes in colon of antagomir-155 treated mice at day 15. *P < 0.05, vs antagomir-treated NC (Student’s t-test in (B,D,G)]; n = 4–5 per group. Data are representative of two independent experiments (mean and SD). NC, negative control; WT, wild-type.