Colon animal models

Key Words Staphylococcus aureus nasal colonization animal model cotton rat therapy. 

Colon inflammation 1. AEA levels are elevated in the colon of DNBS-treated mice and in the colon submucosa of TNBS-treated rats, two animal models of inflammatory bowel diseases, and in the biopsies of patients with ulcerative colitis, to control inflammation 1. Inhibitors of degradation (both FAAH and cellular re-uptake)... 

Keshavarzian, A., Doria, M.I., Sedghi, S., Kanofeky, J.R., Hecht, D., Holmes, E.W., Ibrahim, C., List, T., Urban, G., Gaginella, T. and Fields, J.Z. (1992a). Mitomycin C-induced colitis in rats a new animal model of acute colonic inflammation implicating reactive oxygen metabolites. J. Lab. Clin. Med. 120, 778-791. 

Experiments conducted in the early 1980s showed that lymphocytes incubated in vitro with IL-2 could subsequently kill a range of cultured cancer cell lines, including melanoma and colon cancer cells. These latter cancers do not respond well to conventional therapies. Subsequent investigations showed that cancer cell destruction was mediated by IL-2-stimulated NK cells (i.e. LAK cells). Similar responses were seen in animal models upon administration of LAK cells activated in vitro using IL-2. 

Although there are preliminary data supporting the antitumoral activity of quercetin, the most common flavonoid, in humans in the course of a Phase I clinical trial [189], direct evidence of the anticancer effect of flavonoids is derived almost exclusively from studies performed in animal models as well as studies performed on cultured cell lines, Fig. (2). Most animal studies on gastrointestinal cancer have focused on colon cancer using the azoxymethane (AOM) model in rats or mice [190-197]. There are also available reports on models of cancer of the stomach (induced by benzo[a]pyrene [198] or N-methyl-N-nitro-N-nitro so guanidine [199]), oesophagus (N-methyl-N-amylnitrosamine [200]), and the tongue/oral cavity (methyl-(acetoxymethyl)-nitrosamine [198], 7,12-dimethyl-... 

The possible role of dietary fat on colon carcinogenesis has received support from studies in animal models. In several earlier studies on dietary fat and colon cancer, interpretation of results between high- and low-fat diets was complicated by the use of diets of varying caloric density and confounded by different intakes of other nutrients. However, recent studies in which the intake of all nutrients and total calories were controlled between the high-fat and low-fat groups, indicated that the amount of dietary fat is an important factor in colon carcinogenesis (27). 

Thus, the excretory pattern of fecal secondary bile acids observed in these studies correlated with colon tumor incidences in animal models. These studies also suggest that high dietary intake of certain types of fat may be necessary for the full expression of risk for colon cancer. 

Current research in animal models which suggests that the carcinogenic response to a variety of colon carcinogens is enhanced by the dietary fat and inhibited by several dietary fibers, indicates that these nutritional factors may operate during the promotional phase of carcinogenesis. The carcinogenic process in humans may... 

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