Fig. 2
Characteristics of a murine model of CAC and the possibility of probiotic treatment in the prevention of CAC. A-left, Stereomicroscopic observation of a murine model of DSS-induced CAC. CAC was induced in BALB/c mice by nine cycles of treatment with 4–5 % DSS in drinking water for 7 days and normal drinking water for 7 days. The arrow indicates CAC. a-right, Histology of CAC. CAC tissue was fixed and stained with H&E. B-left, Expression of IL-6 and SOCS3 mRNA. Total RNA was isolated from colon tissues of chronic colitis or CAC mice. Quantitative RT-PCR was performed using specific primer sets. The data are represented as the mean ± SD (n = 10). b-right, Expression of phosphorylated transcription factors in the mucosa of colitis or CAC mucosa. Colonic tissue homogenates were subjected to Western blotting with polyclonal antibodies against phospho-Stat3, phospho-SHP-2, phospho-Stat1, phospho-NFκB and phospho-38MAPK. C-left, Incidence of CAC. During the induction of CAC, sgp130Fc (500 or 50 μg/mouse) or vehicle was injected i.p. into BALB/c mice on the first day of each 6–9 DSS cycle (n = 10). c-right, Western blot analysis of phospho-Stat3, phospho-NFκB, TACE, phospho-38MAPK and β-catenin in colonic tissue of sgp130Fc- or vehicle- treated mice. D-left, Incidence and number of CAC. During CAC induction, the mice were treated with LcS, PS-PG1-deficient LcS (LCΔPS-PG1) or Saline orally (5 days per week). d-right, Quantitative RT-PCR analysis of IL-6 and SOCS3 mRNA in colonic tissues in CAC-induced mice treated with LcS, LCΔPS-PG1, or PBS. *;p < 0.05, **;p < 0.01, a;p < 0.05, aa;p < 0.01 LcS versus Ct, c;p < 0.05, cc;p < 0.01 LcS versus LCΔP-SPG1