Effect of vitamin C on azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced colitis-associated early colon cancer in mice.
10.4162/nrp.2018.12.2.101
- Author:
Hee Jin JEON
1
;
Yiseul YEOM
;
Yoo Sun KIM
;
Eunju KIM
;
Jae Ho SHIN
;
Pu Reum SEOK
;
Moon Jea WOO
;
Yuri KIM
Author Information
1. Department of Nutritional Science and Food Management, Ewha Womans University, 52 Ewhayeodae-gil, Seodaemun-gu, Seoul 03760, Korea. yuri.kim@ewha.ac.kr
- Publication Type:Original Article
- Keywords:
Vitamin C;
colitis;
inflammation;
colonic neoplasm;
microbiota
- MeSH:
Animals;
Ascorbic Acid*;
Azoxymethane*;
Body Weight;
Colitis;
Colon*;
Colonic Neoplasms*;
Cyclooxygenase 2;
Cytokines;
Drinking Water;
Dysbiosis;
Gastrointestinal Microbiome;
Humans;
Inflammation;
Interleukin-6;
Interleukins;
Lactococcus;
Male;
Mice*;
Microbiota;
Necrosis;
Proliferating Cell Nuclear Antigen;
RNA, Messenger;
Sodium*;
Vitamins*
- From:Nutrition Research and Practice
2018;12(2):101-109
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND/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-α, Interleukin (IL)-1β, 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.
