VSL#3 Prevents Ulcerative Colitis Carcinogenesis in Mice and Cell by Regulating Inflammatory and Wnt/β-catenin Pathway
: The exact mechanism of how VSL#3 prevents ulcerative colitis (UC) carcinogenesis is still not clear. We aimed to explore the effect and mechanism of VSL#3 on UC carcinogenesis in mice and cell. Methods: In mice, C57BL/6 mice were given azoxymethane/dextran sulfate sodium to establish the UC carcinogenesis model. The treatment groups received 5-ASA, VSL#3, 5-ASA combined with VSL#3 by gavage. The tumor load was compared in each group. TNF-α, IL-6 levels in colon tissue, the transcription
... transcription activity of NF-κB and TCF-4 as well as the β-catenin distribution in the nuclei were assessed. In cell, Caco-2 cells, CCC-HIE-2 cells was co-cultured with Bi dobacterium, and was stimulated by IL-6 and TNF-α respectively. The relative luciferase activity, mRNA and protein level of β-catenin, expression of β-catenin in nucleoprotein, level of in ammatory factors, and transcriptional activity of NF-κB and TCF-4 was measured. Results: In mice, compared with the model control group, in VSL#3 and 5-ASA+VSL#3 groups, the tumor loads signi cantly decreased, the TNF-α and IL-6 level, the transcription activity of NF-κB, β-catenin expression in the nuclei, and transcription activity of TCF-4 were signi cantly lower. In cell, the level of TNF-α and IL-6 was down-regulated, transcription activities of NF-κB and TCF-4 were decreased, and the expression level of β-catenin in nucleus was distinctly declined in the Bi dobacterium co-culture group compared with non-co-culture group. Conclusion: VSL#3 inhibit tumor formation in UC carcinogenesis mice model by regulating in ammatory and Wnt/β-catenin Pathway. Similarly, Bi dobacterium co-culture can inhibit the activity of Wnt/β-catenin pathway in cell.