5,7-Dimethoxyflavone enhances barrier function by increasing occludin and reducing claudin-2 in human intestinal Caco-2 cells

Journal of Functional Foods

卷:85

Mayu Okudaira¹  Yunika Mayangsari²  Chinatsu Mano³  Takuya Suzuki³  Yoshinari Yamamoto⁴  Osamu Ueda⁴  Yoshiharu Suzuki⁴  Tomohiro Sakuta⁴  Yuki Tanaka⁴ 

[1] Faculty of Agricultural Technology, Gadjah Mada University, Jl. Flora No 1, Depok, Sleman, Yogyakarta 55281, Indonesia;

[2] Graduate School of Biosphere Science, Hiroshima University, 1-4-4 Kagamiyama, Higashi-Hiroshima 739-8528, Japan;

[3] Graduate School of Integrated Sciences for Life, Hiroshima University, 1-4-4 Kagamiyama, Higashi-Hiroshima 739-8528, Japan;

[4] Shiseido Global Innovation Center. 1-2-11 Takashima, Nishi-ku, Yokohama 220-0011, Japan;

关键词: Claudin;    Dimethoxyflavone;    microRNA;    Occludin;    Tight junction;   

DOI  :  

来源: DOAJ

【 摘 要 】

Defects in intestinal tight junction (TJ) barrier cause intestinal inflammation. We investigated the effects of 5,7-dimethoxyflavone (DMF), abundantly found in black ginger, on the TJ barrier in human intestinal Caco-2 cells. DMF reinforced TJ barrier integrity, indicated by increased transepithelial electrical resistance and reduced dextran permeability in Caco-2 cells. Immunoblot analysis revealed that the increases in the barrier-forming TJ molecules occludin and claudin-1 and the decrease in pore-forming claudin-2 in the cytoskeletal fraction of the cells were responsible for the TJ regulation. Increased occludin expression was sensitive to cycloheximide (an inhibitor of protein translation) and rapamycin (mechanistic target of rapamycin [mTOR] inhibitor). DMF reduced Cldn2 mRNA levels without suppressing its transcriptional activity; the reduction was associated with the upregulation of miR-16-5p. Thus, DMF-mediated reinforcement of intestinal TJ barrier was partly involved in the induction of occludin protein translation via mTOR and silencing Cldn2 mRNA via miR-16-5p.

【 授权许可】

Unknown