Supplemental Naringenin Prevents Intestinal Barrier Defects and Inflammation in Colitic Mice

Abstract

Intestinal barrier defects are involved in the pathogenesis of inflammatory bowel disease. The present study investigated the ameliorative effects of naringenin, a citrus polyphenol, on intestinal tight junction (TJ) barrier defects and inflammation in a murine model of colitis. In Expt. 1, using a 2 × 2 fractional design, the mice were administered water or 2% dextran sulfate sodium (DSS) in combination with feeding control or naringenin-containing diets for 9 d (severe disease stage). DSS administration caused severe colon damage and inflammation, as indicated by body weight loss, increased clinical sores, colon shortening, and gene expressions of inflammatory cytokines [interferon-γ, interleukin (IL)-6, macrophage inflammatory protein-2, and IL-17A). DSS administration also impaired TJ barrier integrity in the colon, as indicated by increased colon permeability and plasma LPS-binding protein levels, resulting from the impaired colonic expression of TJ proteins, occludin, junctional adhesion molecule-A, and claudin-3. Supplemental feeding with naringenin totally or partially attenuated these symptoms, suggesting that naringenin ameliorates the DSS-induced colitis at least partially through protection of the TJ barrier. In Expt. 2, analyses were performed at different disease stages (d 3, 6, and 9) to more widely examine the ameliorative role of naringenin on the initiation and development of colitis. DSS administration moderately induced colon shortening at d 3 and 6 and increased the disease activity index (DAI) and inflammatory cytokine (IL-6 and IL-17A) expression without any significant increases in colonic permeability. Feeding naringenin attenuated the increased DAI and colon shortening and tended to suppress the increased cytokine expression. These findings suggest that the presence of an additional mechanism underlying the naringenin-mediated, anticolitic effect along with barrier protection.

Isomaltodextrin Prevents DSS-induced Colitis by Strengthening Tight Junctions in Mice

“…Immunohistochemical detection of claudin-3 expression in the colon of DSS-colitis mice cytokines, such as IL-6 and IL-17A. As a result, the DSS-induced colitis was mitigated (Azuma et al, 2013).…”

“…For example, lowered protein levels of ZO-1 and claudin-3 have been noted, leading to an increase in intestinal epithelium permeability. Meanwhile, because the gastrointestinal epithelium is continuously exposed to food components in the lumen, TJ regulation may be modified by these components (Azuma et al, 2013). Therefore, in the present study, we investigated the effects of isomaltodextrin (IMD) as one such component on TJs.…”

“…Subsequently, lysis buffer (Azuma et al, 2013) was added to the frozen tissues (1 mL/30 mg tissue), which were minced with scissors, disrupted using a Polytron-type homogenizer, heated at 95℃ for 5 min, and centrifuged at 13,000 rpm and 4℃…”

Enhancing Effect of Trachelogenin from <i>Trachelospermi caulis</i> Extract on Intestinal Barrier Function

“…Furthermore, naringenin has been shown to protect against impairment of the intestinal barrier and inflammation in a dextran sulfate sodium-induced model of colitis. 25) These reports showed that food-or herb-derived components such as a naringenin could prevent intestinal inflammation (e.g., IBD) through enhancement of intestinal barrier function. Our results showed the enhancing effect of T. caulis on intestinal barrier function, and that T. caulis could contribute to attenuate food allergy.…”

Impact of epigallocatechin-3-gallate (EGCG), a broad-spectrum anti-inflammatory, in controlling intestinal factors contributing to inflammatory bowel disease.

“…Examination of TER data presented in this paper clearly demonstrates that EGCG increases epithelial electrical resistance and TJ protein expression levels after 18-24 hours of incubation with Caco-2 cell monolayers. These data suggest an additional mechanism underlying EGCG-mediated protection against colitis (Azuma, Shigeshiro et al 2013). Future studies on the anti-inflammatory effects of EGCG should evaluate its impact on the regulation, expression, and function of barrier related components in clinical subjects with IBD.…”