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Effect of vitamin C on azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced colitis-associated early colon cancer in mice

  • Jeon, Hee-Jin (Department of Nutritional Science and Food Management, Ewha Womans University) ;
  • Yeom, Yiseul (Department of Nutritional Science and Food Management, Ewha Womans University) ;
  • Kim, Yoo-Sun (Department of Nutritional Science and Food Management, Ewha Womans University) ;
  • Kim, Eunju (Department of Nutritional Science and Food Management, Ewha Womans University) ;
  • Shin, Jae-Ho (Department of Biomedical Laboratory Science, Eulji University) ;
  • Seok, Pu Reum (Department of Biomedical Laboratory Science, Eulji University) ;
  • Woo, Moon Jea (Kwang-Dong Pharmaceutical Co., Ltd.) ;
  • Kim, Yuri (Department of Nutritional Science and Food Management, Ewha Womans University)
  • Received : 2017.12.14
  • Accepted : 2018.02.08
  • Published : 2018.04.01

Abstract

BACKGROUD/OBJECTIVES: The objective of this study was to investigate the effects of vitamin C on inflammation, tumor development, and dysbiosis of intestinal microbiota in an azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced inflammation-associated early colon cancer mouse model. MATERIALS/METHODS: Male BALB/c mice were injected intraperitoneally with AOM [10 mg/kg body weight (b.w)] and given two 7-d cycles of 2% DSS drinking water with a 14 d inter-cycle interval. Vitamin C (60 mg/kg b.w. and 120 mg/kg b.w.) was supplemented by gavage for 5 weeks starting 2 d after the AOM injection. RESULTS: The vitamin C treatment suppressed inflammatory morbidity, as reflected by disease activity index (DAI) in recovery phase and inhibited shortening of the colon, and reduced histological damage. In addition, vitamin C supplementation suppressed mRNA levels of pro-inflammatory mediators and cytokines, including cyclooxygenase-2, microsomal prostaglandin E synthase-2, tumor necrosis $factor-{\alpha}$, Interleukin $(IL)-1{\beta}$, and IL-6, and reduced expression of the proliferation marker, proliferating cell nuclear antigen, compared to observations of AOM/DSS animals. Although the microbial composition did not differ significantly between the groups, administration of vitamin C improved the level of inflammation-related Lactococcus and JQ084893 to control levels. CONCLUSION: Vitamin C treatment provided moderate suppression of inflammation, proliferation, and certain inflammation-related dysbiosis in a murine model of colitis associated-early colon cancer. These findings support that vitamin C supplementation can benefit colonic health. Long-term clinical studies with various doses of vitamin C are warranted.

Keywords

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