Introduction
Inflammatory bowel disease (IBD) is a complex chronic and relapsing inflammatory disorder of the gastrointestinal tract with unclear pathogenesis. Accumulating evidence suggests food emulsifiers as a risk factor for the development of IBD. It is indicated that food emulsifiers carboxymethylcellulose (CMC) can alter gut microbiota and promote intestinal inflammation in IBD under normal diet. Since high-fat diet is the main life scenario for CMC use, little is known about the effect of CMC on colitis model in different high-fat diet.
Aims & Methods
C57/BL6 mice (3-5 weeks old) were randomly divided into three high-fat diet (HFD) groups, which only differed by fat composition (40 %), derived from corn oil (HCO, n-6 polyunsaturated fatty acids), olive oil (HOO, monounsaturated fatty acids) and milk fat (HMF, saturated fatty acids), and exposed to CMC (1.0% w/v) in drinking water for 4 weeks before the establishment of dextran sulfate sodium (DSS) induced acute colitis mice model. Colon inflammation severity was evaluated using survival rate, HE staining, colon length, body weight change and DAI score. Ki67 and TUNEL assays were performed to detect proliferation and apoptosis.
Results
Compared with the CMC+DSS group, the HMF+CMC+DSS group markedly increased survival rate (P=0.013), colon length (P=0.027) and body weight (day4, day5, day6 and day7, P<0.05, respectively), and relieved DAI score (day4 and day6, P<0.05, respectively) and histological damage (P<0.0001). The HOO+CMC+DSS group seemly had no significant difference from the CMC+DSS group. In contrast, the HCO+CMC+DSS group developed more aggressive colitis with increased DAI score (day5, P<0.01) and decreased body weight (day1, day2, day5 and day6, P<0.05, respectively). In terms of maintaining homeostasis of the intestinal barrier, the HMF+CMC+DSS group showed the highest Ki67 (P=0.012, P=0.0002 P=0.042, respectively) and TUNEL positive cells (P=0.324, P<0.0001, P<0.0001, respectively) compared with the CMC+DSS, HOO+CMC+DSS or HCO+CMC+DSS group. Between CMC+DSS and HOO+CMC+DSS or HCO+CMC+DSS group, there was no difference in Ki67 positive cells, while TUNEL positive cells significantly decreased (P=0.002, P=0.008, respectively).
Conclusion
The function of CMC on DSS colitis varies in different high-fat. Unexpectedly, CMC protects against the development of high-milk-fat related colitis by maintaining homeostasis of proliferation and apoptosis.
References
The function of CMC on DSS colitis varies in different high-fat. Unexpectedly, CMC protects against the development of high-milk-fat related colitis by maintaining homeostasis of proliferation and apoptosis.
Disclosure
none
