3,3'-Diindolylmethane improves intestinal permeability dysfunction in cultured human intestinal cells and the model animal Caenorhabditis elegans
- Title
- 3,3'-Diindolylmethane improves intestinal permeability dysfunction in cultured human intestinal cells and the model animal Caenorhabditis elegans
- Authors
- 차광현; 강경수; 판철호; 송대근; 이재욱; 홍성철; 김주연; 레 응옥 트람 안; 이소영
- Keywords
- Caenorhabditis elegans; 3,3′-diindolylmethane; inflammatory bowel disease; interleukin-1β; intestinal permeability
- Issue Date
- 2019-08
- Publisher
- Journal of agricultural and food chemistry
- Citation
- VOL 67, NO 33-9285
- Abstract
- 3,3′-Diindolylmethane (DIM), a digestive metabolite originating from cruciferous vegetables, has dietary potential for the treatment of various human intestinal diseases. Although intestinal permeability dysfunction is closely related to the initiation and progression of human intestinal inflammatory diseases (IBDs), the effect of DIM on intestinal permeability is unclear. We evaluated the effect of DIM on the intestinal permeability of human intestinal cell monolayers and the animal model Caenorhabditis elegans, which were treated with IL-1β and Pseudomonas aeruginosa, respectively, to mimic IBD conditions. DIM substantially restored the intestinal permeability of differentiated Caco-2 cells by enhancing the expression of tight junction proteins (including occludin and ZO-1). Compared to the IL-1β single treatment (551.0 ± 49.0 Ω·cm2), DIM (10 μM) significantly increased the transepithelial electrical resistance (TEER) of Caco-2 cell monolayers (919.0 ± 66.4 Ω·cm2, p < 0.001). DIM also ameliorated the impaired intestinal permeability and extended the lifespan of C. elegans fed P. aeruginosa. The mean lifespan of DIM-treated worms (10.8 ± 1.3 days) was higher than that of control-treated worms (9.7 ± 1.1 days, p < 0.01). Thus, DIM is a potential nutraceutical candidate for the treatment of leaky gut syndrome by improving intestinal permeability.
- URI
- https://pubs.kist.re.kr/handle/201004/69874
- ISSN
- 0021-8561
- Appears in Collections:
- KIST Publication > Article
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