Fig. 7

Inosine protects against dextran sulfate sodium (DSS)-induced colitis through the A_2AR/PPARγ signaling pathway. a–n Mice were treated intragastrically with 800 mg/kg/day of inosine dissolved in PBS at the concentration of 40 mg/ml. PPARγ antagonist GW9662 were administered at 3 mg/kg/day intragastrically and A_2AR antagonist SCH58261 were treated with 2 mg/kg/day intraperitoneally. Colitis was induced by administering 2.5% DSS dissolved in drinking water for 7 days. a Study design of in vivo mouse experiment. b Immunofluorescent analysis of PPARγ (green) in mouse colonic sections from different mouse groups. Nuclei were stained with DAPI (blue). Scale bar = 100 μm. c Real-time PCR assay for the differentially expressed genes in PPAR signaling pathway (n = 8). d Crypt height and e muscular layer width in the colon of mice from different mouse groups were quantified (n = 12). f Fecal pellet output and g gut transit time from different mouse groups were measured (n = 8). h Representative alcian blue-stained and Muc2-stained colon sections from different mouse groups. The number of mucus­producing goblet cells and Muc-2-positive goblet cells was quantified (n = 12). Scale bar = 100 μm. i Percentage body weight change, j diseases activity scores, k colon lengths, and l intestinal permeability were measured from different mouse groups (n = 8). m Representative images of hematoxylin and eosin-stained colonic sections and n histological scores. Scale bar = 100 μm. Data are pooled from three independent experiments. Data are mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 and ****P < 0.0001. For body weight change, a repeated measure two-way analysis of variance (ANOVA) was performed and the rest of the statistics was performed with one-way ANOVA followed by Tukey’s multiple comparisons test