During the acute phase (Day 14), H&E staining colon tissue from model animals showed: increasingly

severe inflammatory lesions extensively throughout the colon; significant and complete loss of crypts; surface erosion with exuberant inflammatory exudates; patchy re-epithelization; lamina propria fibrosis with acute and chronic Proteasome inhibitor inflammatory infiltrate; submucosal edema; and mixed inflammatory cell infiltration. In the AG group, mucosa had tightly packed glands with a normal amount of goblet cells (Fig. 3A). The disease severity, scored by the DAI, reached its highest level on Day 8. Fig. 3B shows significant effects of AG on the reduction of the DAI score (p < 0.05). This suppression of the experimental colitis by the herb was not only evident during DSS treatment, but also very obvious after the cessation of DSS administration (i.e., Day 8), suggesting that AG significantly promoted recovery from the colitis. Fig. 4A is a representative macroscopic morphology for the control group, model group, and AG group. Obvious tumorigenesis was observed

in the model group. However, in the AG treatment group, the tumor number and size were significantly less and relative small. Fig. 4B shows representative find more H&E staining histological sections of the three groups. In the colon tissue from the model animals, multifocal adenomatous lesion was observed, and there was no invasion into submucosa; there was mild inflammation with cryptitis, mild degree loss of goblet cells, fibrosis, and apoptotic changes. For the AG treatment group, mucosa shows tightly packed glands with a normal amount of goblet cells while crypt architecture remained normal. Compared to the model, the histological sections of the AG treatment group are more similar to those science of the control group. Fig. 4C shows colon carcinogenesis data. Our results showed that compared to the model group, AG treatment very significantly reduced the total number of colon tumors and load of tumors (p < 0.01 and p < 0.001, respectively). Tumor distribution data reflected this reduction, in which the number of large tumors (1–2 mm and > 2 mm) decreased while the number

of small tumors (< 1 mm) increased. Previous studies have shown that blockade of inflammatory cytokines significantly decrease the severity of colitis. To explore mechanisms of inhibition of AOM/DSS induced colitis and tumorigenesis by AG treatment, using an ELISA array, we determined proinflammatory cytokine levels in the colon tissues collected on Day 14. Colonic levels of the proinflammatory cytokines IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, IL-12, IL-17A, IFN-γ, tumor necrosis factor-α, G-CSF, and GM-CSF were markedly elevated in the DSS model group. Treatment with AG significantly inhibited the levels of those 12 cytokines by 44%, 35%, 42%, 39%, 46%, 34%, 37%, 44%, 51%, 40%, 46%, and 37%, respectively (p < 0.05; Fig. 5).