A diet with lactosucrose supplementation ameliorates trinitrobenzene sulfonic acid-induced colitis in rats.

Abstract

Chronic intestinal inflammation contributes to an increased risk of colon cancer. Lactosucrose (LS), a kind of functional trisaccharide, can modulate immunity and promote microbe growth. The aim of this study was to investigate the effect of LS on 2,4,6-trinitrobenzene sulfonic acid (TNBS) induced colitis in rats. Rats were randomly divided into four treatment groups: the normal group, TNBS group, LS group, and salicylazosulfapyridine (SASP) group for five weeks. LS supplementation ameliorated TNBS-induced colitis. LS supplementation increased IL-10 production and suppressed the secretion of IL-12 in the colon, as compared to the TNBS group. LS decreased the production of TLR-2 protein and nuclear NF-κB p65 protein, as well as mRNA levels, as compared with colitic rats. These results indicate that chronic feeding of LS inhibited TNBS-induced chronic inflammation. LS has potential nutraceutical intervention to combat colitis.

• Authors: Yan Zhou, Zheng Ruan, Xiaoli Zhou, Xiaoliu Huang, Hua Li, Ling Wang, Cui Zhang, Shiqiang Liu, Zeyuan Deng, Guoyao Wu, Yulong Yin
• Journal: Food & function (Food Funct) Vol. 6 Issue 1 Pg. 162-72 (Jan 2015) ISSN: 2042-650X [Electronic] England
• PMID: 25367079 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Anti-Inflammatory Agents, Non-Steroidal
• Gastrointestinal Agents
• Prebiotics
• Rela protein, rat
• Tlr2 protein, rat
• Toll-Like Receptor 2
• Transcription Factor RelA
• Trisaccharides
• Interleukin-10
• Interleukin-12
• Sulfasalazine
• galactosucrose
• Trinitrobenzenesulfonic Acid

Topics

• Animals
• Anti-Inflammatory Agents, Non-Steroidal (therapeutic use)
• Colitis (diet therapy, metabolism, pathology)
• Colon (immunology, metabolism, pathology)
• Disease Models, Animal
• Female
• Gastrointestinal Agents (therapeutic use)
• Inflammatory Bowel Diseases (diet therapy, metabolism, pathology)
• Interleukin-10 (agonists, metabolism)
• Interleukin-12 (antagonists & inhibitors, metabolism)
• Intestinal Mucosa (immunology, metabolism, pathology)
• Prebiotics
• Random Allocation
• Rats, Sprague-Dawley
• Specific Pathogen-Free Organisms
• Sulfasalazine (therapeutic use)
• Toll-Like Receptor 2 (antagonists & inhibitors, genetics, metabolism)
• Transcription Factor RelA (antagonists & inhibitors, genetics, metabolism)
• Trinitrobenzenesulfonic Acid
• Trisaccharides (therapeutic use)