Abstract

This study examines the ameliorative effects of lemon (Citrus limon) peel (LP) powder on intestinal inflammation and barrier defects in dextran sulfate sodium (DSS)-induced colitic mice. The whole LP powder was fractionated into methanol (MetOH) extract and its extraction residue (MetOH residue), which were rich in polyphenolic compounds and dietary fibers, respectively. Mice were fed diets containing whole LP powder, MetOH extract, and MetOH residue for 16 d. DSS administration for 9 d induced bodyweight loss, reduced colon length, reduced the colonic expression of tight junction proteins including zonula occludens-1 and -2, and claudin-3 and -7, and upregulated colonic mRNA expression of interleukin 6, chemokine (C-X-C motif) ligand 2, and C-C motif chemokine ligand 2. Feeding LP powder restored these abnormalities, and the MetOH residue, but not MetOH extract, also showed similar restorations. Feeding LP powder and MetOH residue increased fecal concentrations of acetate and n-butyrate. Taken together, LP powder reduced intestinal damage through the protection of tight junction barriers and suppressed an inflammatory reaction in colitic mice. These results suggest that acetate and n-butyrate produced from the microbial metabolism of dietary fibers in LP powder contributed to reducing colitis.

Highlights

  • Published: 25 January 2021Inflammatory bowel diseases (IBDs) mainly consist of ulcerative colitis and Crohn’s disease, which are chronic idiopathic disorders causing intestinal inflammation [1]

  • This study demonstrated that whole lemon peel (LP) powder, rich in polyphenolic compounds and dietary fibers, attenuated an intestinal barrier defect and inflammation in a murine model of colitis

  • This study examined the ameliorative effects of LP powder on intestinal inflammation and barrier defects, and the bioactive components responsible for the effect were examined in dextran sodium sulfate (DSS)-induced colitic mice

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Summary

Introduction

Inflammatory bowel diseases (IBDs) mainly consist of ulcerative colitis and Crohn’s disease, which are chronic idiopathic disorders causing intestinal inflammation [1]. South America, eastern Europe, Asia, and Africa [2]. These data suggest that both genetic and environmental factors, such as dietary habits, are involved in IBD pathogenesis. IBD pathogenesis is not fully understood, data from basic and clinical studies show that an impaired intestinal barrier triggers intestinal inflammation [3]. An impaired intestinal barrier allows noxious molecules, such as bacterial toxins and dietary antigens, to permeate intestinal tissues, resulting in the robust and chronic activation of immune cells [3]. The TJ structure is a multiple protein complex, consisting of transmembrane and cytosolic plaque proteins, including the transmembrane proteins, occludin, and claudins, whose extracellular loops directly interact with

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