Expression of the methylcytosine dioxygenase ten-eleven translocation-2 and connexin 43 in inflammatory bowel disease and colorectal cancer

Figure 4 Dextran sulfate sodium induces inflammation in mice and carbenoxolone restores the normal phenotype. A: A flowchart schematizing the in vivo experimental design. BALB/c male mice were distributed into four experimental groups, each comprised of five mice: (1) Control group that received normal drinking water with no carbenoxolone (CBX) injections; (2) CBX group that received normal drinking water with CBX injections starting day 11; (3) Dextran sulfate sodium (DSS) group where mice were administered with 2.5% DSS in their drinking water for 10 d but not subjected to any CBX injections; and (4) DSS + CBX group that received DSS-containing drinking water as well as CBX injections. Mice were given 30 mg/kg CBX via intraperitoneal injections from day 11 every other day to the end of the experiment; B: Variation of animal body weight over 21 d. DSS-exposed mice lost weight. Significance in body weight change was detected between days 4 and 12 in DSS-treated mice, and days 11 and 21 in CBX-injected mice only; C: Hematoxylin and eosin images showing the architecture of mice colon tissues from all experimental groups. Arrows indicate representative sites in each experimental condition. Scale bar 50 μm; D: Colon length was measured at the end of the experiment. DSS-treated mice showed significantly longer colons compared to the control group; E: Bar graphs showing the normalized gene expression of interleukin-1β and tumor necrosis factor-α in mouse colon tissues, as detected by quantitative polymerase chain reaction. Experiments were repeated five times and results are displayed as means ± SEM. One-way ANOVA, ^aP < 0.05. IL: Interleukin; CBX: Carbenoxolone; DSS: Dextran sulfate sodium; TNF-α: Tumor necrosis factor-α.