Abstract
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-β activity. These results suggest that FRB may be an alternative therapeutic agent against inflammation-induced intestinal fibrosis.
Highlights
Inflammatory bowel disease (IBD) is characterized by diarrhea, bloody stools, abdominal pain, and weight loss
These results suggest that rice bran (RB) and Fermented rice bran (FRB) supplementation might be able to prevent intestinal fibrosis due to dextran sodium sulfate (DSS)-induced inflammation via the regulation of Smad 2/3 protein level
We found no statistical differences in the mRNA levels of Tgf-β1 with diet treatments among all the groups (Figure 8C); the combined effect of Tgf-β and other cytokines and chemokines might have been a crucial factor in the deposition of extracellular matrix (ECM) in the intestinal lining, which will affect the onset of fibrosis after DSS-induced inflammation
Summary
Inflammatory bowel disease (IBD) is characterized by diarrhea, bloody stools, abdominal pain, and weight loss. IBD was originally considered to manifest in genetically vulnerable individuals, and there are currently 163 loci known to contribute to the onset of IBD. Examples of these genes are NOD2 (which is related to innate sensing of bacteria) [2,4], IL23R (which regulates inflammatory response to microbes) [2], CARD9 (which integrates signals from innate immune receptors and activates different pathways of cytokines in response) [5], and ATG16L1 (which controls autophagy) [2]. Apart from genetic factors, environmental factors such as smoking, hygiene, dietary intake, and antibiotics usage are considered to affect the onset of IBD [4]
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