To validate inflammatory cytokine data observed in the ELISA analysis, we examined the effect of AG on the expression of inflammatory cytokine

genes in both the acute (Day 14) and chronic (Day Galunisertib research buy 90) phases. We used RT-PCR to test the effects of AG on the target genes in colon tissues, which were collected on Day 14 and Day 90. As shown in Fig. 6A, in the acute phase (Day 14), the expression of six inflammatory cytokines (IL-1α, IL-1β, IL-6, IFN-γ, G-CSF, and GM-CSF) in the model group is much higher than in the control group (all p < 0.001). Compared to the model, ginseng treatment significantly downregulated the expression of the tested inflammatory cytokines (all p < 0.01). In the chronic phase (Day 90), similar effects were also observed, and AG treatment more significantly inhibited inflammatory cytokine expression (all p < 0.001 vs. model; Fig. 6B). This result indicate that the oral administration of AG transcriptionally repressed inflammatory cytokines in the gut tissue. Colorectal cancer is the second leading cause of cancer-related

death in the West [2] and [23]. This cancer also remains a foremost cause of morbidity and mortality, a significant contributor to the burden of disease of global public health. Inflammatory bowel disease, including ulcerative colitis and Crohn’s disease, is a risk factor for colon cancer initiation and development [10] and [11]. Nonsteroidal anti-inflammatory selleckchem drugs can reduce colon cancer tumorigenesis. For example, celecoxib has potent preventive and therapeutic effects on the cancer [24]. Concerns about the risks of long-term use of such drugs, however, make

this form of chemoprevention unsuitable as a general recommendation [25] and [26]. Epidemiological, experimental, and clinical studies provide evidence that inflammatory phytochemicals possess unique modes of action against cancer development and growth PRKACG [27], [28] and [29]. In the present study, the effects of AG were investigated, as one of the efforts to search for the botanical sources against this significant medical problem. Experimentally, AOM (a mutagenic agent) and/or DSS (a proinflammatory reagent) have often been used in colorectal cancer chemoprevention animal studies [15], [30], [31] and [32]. In this study we used the AOM/DSS mouse model to mimic the inflamed colon and carcinogenesis conditions in humans [15] and [33]. There were two observation phases in this study. The acute phase (Day 1–14) reflected the manifestation of inflammatory colitis, measured by DAI (Fig. 3). The chronic phase (up to 90 days) revealed the colon carcinogenesis (Fig. 4), measured by colon tumor number and tumor load. Compared with the model group, we observed that AG treatment significantly attenuated the experimental colitis.