4.7 Article

Fermented Rice Bran Supplementation Prevents the Development of Intestinal Fibrosis Due to DSS-Induced Inflammation in Mice

Journal

NUTRIENTS
Volume 13, Issue 6, Pages -

Publisher

MDPI
DOI: 10.3390/nu13061869

Keywords

colitis; dextran sodium sulfate; fermented rice bran; intestinal fibrosis; intestinal inflammation

Funding

  1. JSPS Core-to-Core Program A (Advanced Research Networks)
  2. Kobayashi Foundation
  3. Tojuro Iijima Foundation for Food Science and Technology
  4. Salt Science Research Foundation [20D4]
  5. Joint Projects of Rice Bran of Sunstar Inc.

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The study showed that dietary FRB supplementation can promote intestinal restoration after DSS-induced colitis and reduce the development of intestinal fibrosis. FRB supplementation also decreased the severity of colitis, increased levels of anti-inflammatory cytokines, tight junction proteins, and antimicrobial proteins in the intestines.
Fermented rice bran (FRB) is known to protect mice intestines against dextran sodium sulfate (DSS)-induced inflammation; however, the restoration of post-colitis intestinal homeostasis using FRB supplementation is currently undocumented. In this study, we observed the effects of dietary FRB supplementation on intestinal restoration and the development of fibrosis after DSS-induced colitis. DSS (1.5%) was introduced in the drinking water of mice for 5 days. Eight mice were sacrificed immediately after the DSS treatment ended. The remaining mice were divided into three groups, comprising the following diets: control, 10% rice bran (RB), and 10% FRB-supplemented. Diet treatment was continued for 2 weeks, after which half the population of mice from each group was sacrificed. The experiment was continued for another 3 weeks before the remaining mice were sacrificed. FRB supplementation could reduce the general observation of colitis and production of intestinal pro-inflammatory cytokines. FRB also increased intestinal mRNA levels of anti-inflammatory cytokine, tight junction, and anti-microbial proteins. Furthermore, FRB supplementation suppressed markers of intestinal fibrosis. This effect might have been achieved via the canonical Smad2/3 activation and the non-canonical pathway of Tgf-beta activity. These results suggest that FRB may be an alternative therapeutic agent against inflammation-induced intestinal fibrosis.

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