Mizuki Shigeshiro

Hiroshima University, Hiroshima-shi, Hiroshima-ken, Japan

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Publications (2)9.81 Total impact

  • [Show abstract] [Hide abstract]
    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.
    Journal of Nutrition 04/2013; · 4.20 Impact Factor
  • Mizuki Shigeshiro, Soichi Tanabe, Takuya Suzuki
    [Show abstract] [Hide abstract]
    ABSTRACT: The mucin family plays a number of important roles in intestinal homeostasis. Among its members, the gel-forming Muc2, produced in goblet cells, is a major component of mucus and contributes to intestinal barrier integrity. Whereas psychological stress is known to impair intestinal barrier, the effects of chronic or repeated stress on mucin expression and goblet cell differentiation have not been well documented. The present study first examined the effects of different levels of exposure (3days, 1 and 2weeks) to water immersion stress on intestinal mucin gene expression in rats, and then explored the mechanisms underlying the stress-induced decrease in the colonic Muc2 level. Repeated water immersion stress for 1 and 2weeks decreased colonic Muc2 gene levels to 40% of that of non-stressed animals, while exposure to stress for 3days induced only a 25% decrease. The goblet cell numbers counts in the colons of the 1- and 2-week stress groups, but not the 3-day stress group, were decreased to 85% of that in non-stressed animals. Cdx2 expression, a transcriptional factor related to Muc2 synthesis in the goblet cells, was decreased in all stress groups, whereas Rath1 and Klf4 expressions, transcriptional factors related to goblet cell differentiation in Notch signaling were decreased in the 1-week stress group. Collectively, the repeated exposure to water immersion stress decreases Muc2 synthesis in the goblet cells via decreased Cdx2 expression and subsequently reduces the goblet cell number via Notch signaling suppression.
    Brain Behavior and Immunity 06/2012; 26(7):1061-5. · 5.61 Impact Factor

Publication Stats

3 Citations
9.81 Total Impact Points

Institutions

  • 2012
    • Hiroshima University
      • Department of Biofunctional Science and Technology
      Hiroshima-shi, Hiroshima-ken, Japan