Tags

Type your tag names separated by a space and hit enter

Taxifolin ameliorates lipopolysaccharide-induced intestinal epithelial barrier dysfunction via attenuating NF-kappa B/MLCK pathway in a Caco-2 cell monolayer model.
Food Res Int. 2022 08; 158:111502.FR

Abstract

Intestinal epithelial barrier dysfunction can cause several intestinal diseases. Flavonoids have been shown to be beneficial to the intestinal epithelial barrier function. However, the effects of taxifolin (TAX), a naturally occurring flavonoid, on the intestinal epithelial barrier function are unclear. Thus, the aims of this study were to investigate the protective effect and potential mechanism of TAX against lipopolysaccharide (LPS)-induced intestinal epithelial barrier dysfunction in a Caco-2 cell monolayer model. Our results showed that TAX increased the transepithelial electrical resistance (TEER) and decreased the fluorescein isothiocyanate (FITC)-dextran (4 kDa) flux in the damaged intestinal epithelial barrier. Meanwhile, TAX inhibited an LPS-induced decrease in mRNA and protein expression of tight junction (TJ) proteins (claudin-1, zonula occludens [ZO]-1, and occludin), and ameliorating the continuous distribution pattern disrupted of TJs. These results suggested that TAX ameliorated intestinal epithelial barrier dysfunction. Regarding the underlying mechanism, TAX reduced the LPS-induced secretion of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in Caco-2 cell monolayers. In addition, TAX suppressed the phosphorylation of nuclear factor kappa-B (NF-κB), inhibitor protein of NF-κBα (IκBα), and myosin light chain (MLC), and downregulated the expression of myosin light chain kinase (MLCK) in LPS-treated Caco-2 cells. In summary, TAX can maintain TJ proteins by inhibiting the NF-κB/MLCK pathway and pro-inflammatory factor secretion to ameliorate LPS-induced intestinal epithelial barrier dysfunction. Thus, TAX is a promising candidate agent for use in functional food to ameliorate intestinal barrier dysfunction.

Links

Publisher Full Text (DOI)

Authors+Show Affiliations

College of Food Science, Northeast Agricultural University, Harbin 150030, China.

College of Food Science, Northeast Agricultural University, Harbin 150030, China.

College of Food Science, Northeast Agricultural University, Harbin 150030, China.

College of Food Science, Northeast Agricultural University, Harbin 150030, China.

College of Food Science, Northeast Agricultural University, Harbin 150030, China.

College of Food Science, Northeast Agricultural University, Harbin 150030, China.

College of Food Science, Northeast Agricultural University, Harbin 150030, China; Heilongjiang Green Food Science Research Institute, Northeast Agricultural University, Harbin 150030, China. Electronic address: hanjianchun@hotmail.com.

MeSH

Caco-2 CellsHumansIntestinal DiseasesIntestinal MucosaLipopolysaccharidesMyosin-Light-Chain KinaseNF-kappa BQuercetinTight Junction ProteinsTumor Necrosis Factor-alpha

Pub Type(s)

Journal Article

Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

35840209

Citation

Gong, Shaoying, et al. "Taxifolin Ameliorates Lipopolysaccharide-induced Intestinal Epithelial Barrier Dysfunction Via Attenuating NF-kappa B/MLCK Pathway in a Caco-2 Cell Monolayer Model." Food Research International (Ottawa, Ont.), vol. 158, 2022, p. 111502.

Gong S, Zheng J, Zhang J, et al. Taxifolin ameliorates lipopolysaccharide-induced intestinal epithelial barrier dysfunction via attenuating NF-kappa B/MLCK pathway in a Caco-2 cell monolayer model. Food Res Int. 2022;158:111502.

Gong, S., Zheng, J., Zhang, J., Wang, Y., Xie, Z., Wang, Y., & Han, J. (2022). Taxifolin ameliorates lipopolysaccharide-induced intestinal epithelial barrier dysfunction via attenuating NF-kappa B/MLCK pathway in a Caco-2 cell monolayer model. Food Research International (Ottawa, Ont.), 158, 111502. https://doi.org/10.1016/j.foodres.2022.111502

Gong S, et al. Taxifolin Ameliorates Lipopolysaccharide-induced Intestinal Epithelial Barrier Dysfunction Via Attenuating NF-kappa B/MLCK Pathway in a Caco-2 Cell Monolayer Model. Food Res Int. 2022;158:111502. PubMed PMID: 35840209.

* Article titles in AMA citation format should be in sentence-case

TY - JOUR T1 - Taxifolin ameliorates lipopolysaccharide-induced intestinal epithelial barrier dysfunction via attenuating NF-kappa B/MLCK pathway in a Caco-2 cell monolayer model. AU - Gong,Shaoying, AU - Zheng,Jiachen, AU - Zhang,Junjie, AU - Wang,Yucong, AU - Xie,Zhixin, AU - Wang,Yubao, AU - Han,Jianchun, Y1 - 2022/06/13/ PY - 2022/02/13/received PY - 2022/06/05/revised PY - 2022/06/09/accepted PY - 2022/7/15/entrez PY - 2022/7/16/pubmed PY - 2022/7/20/medline KW - Inflammation KW - Intestinal epithelial barrier KW - MLCK-MLC KW - NF-κB KW - Taxifolin KW - Tight junction SP - 111502 EP - 111502 JF - Food research international (Ottawa, Ont.) JO - Food Res Int VL - 158 N2 - Intestinal epithelial barrier dysfunction can cause several intestinal diseases. Flavonoids have been shown to be beneficial to the intestinal epithelial barrier function. However, the effects of taxifolin (TAX), a naturally occurring flavonoid, on the intestinal epithelial barrier function are unclear. Thus, the aims of this study were to investigate the protective effect and potential mechanism of TAX against lipopolysaccharide (LPS)-induced intestinal epithelial barrier dysfunction in a Caco-2 cell monolayer model. Our results showed that TAX increased the transepithelial electrical resistance (TEER) and decreased the fluorescein isothiocyanate (FITC)-dextran (4 kDa) flux in the damaged intestinal epithelial barrier. Meanwhile, TAX inhibited an LPS-induced decrease in mRNA and protein expression of tight junction (TJ) proteins (claudin-1, zonula occludens [ZO]-1, and occludin), and ameliorating the continuous distribution pattern disrupted of TJs. These results suggested that TAX ameliorated intestinal epithelial barrier dysfunction. Regarding the underlying mechanism, TAX reduced the LPS-induced secretion of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in Caco-2 cell monolayers. In addition, TAX suppressed the phosphorylation of nuclear factor kappa-B (NF-κB), inhibitor protein of NF-κBα (IκBα), and myosin light chain (MLC), and downregulated the expression of myosin light chain kinase (MLCK) in LPS-treated Caco-2 cells. In summary, TAX can maintain TJ proteins by inhibiting the NF-κB/MLCK pathway and pro-inflammatory factor secretion to ameliorate LPS-induced intestinal epithelial barrier dysfunction. Thus, TAX is a promising candidate agent for use in functional food to ameliorate intestinal barrier dysfunction. SN - 1873-7145 UR - https://www.unboundmedicine.com/medline/citation/35840209/Taxifolin_ameliorates_lipopolysaccharide_induced_intestinal_epithelial_barrier_dysfunction_via_attenuating_NF_kappa_B/MLCK_pathway_in_a_Caco_2_cell_monolayer_model_ DB - PRIME DP - Unbound Medicine ER -