Allulose enhances epithelial barrier function by tight junction regulation via the TLR4/MyD88/NF-κB immune signaling pathway in an intestinal Caco-2 cell model

被引:3
|
作者
Baek, Jihye [1 ]
Kim, Jong-Hwa [1 ]
Nam, Yohan [1 ]
Kim, Go-Eun [2 ]
Ryu, Kyungheon [2 ]
Sa, Soonok [2 ]
Han, Jung-Sook [2 ]
Kim, Wonyong [1 ]
机构
[1] Chung Ang Univ, Coll Med, Dept Microbiol, 84 Heukseok Ro, Seoul 06974, South Korea
[2] Samyang Corp, Food R&D Ctr, Seongnam 13488, South Korea
基金
新加坡国家研究基金会;
关键词
D; -allulose; TLR4/MyD88/NF; kappa B signaling; Tight junction; Immune regulation; RARE SUGAR; RECEPTOR; 4; D-PSICOSE; DYSFUNCTION; PROMOTES;
D O I
10.1016/j.jff.2023.105721
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
D-allulose, a fructose isomer with almost zero calories, has been widely used as a food ingredient that is generally recognized as safe. In recent studies, D-allulose has been shown to alleviate some diseases via restoration of the intestinal barrier. To better understand the role of D-allulose in intestinal epithelial barrier function, we conducted experiments to demonstrate its effects. Our results demonstrated that D-allulose increased transepithelial electrical resistance and decreased intestinal barrier function-associated permeability toward 4 kDa FITC-dextran flux in the damaged intestinal epithelial barrier. It also repaired the disruption pattern of tight junction proteins (ZO-1, occludin, and claudin-1) and inhibited the inflammatory response by inhibiting the TLR4/MyD88/NF-kappa B pathway. Overall, these findings suggest that D-allulose has the potential to be a beneficial food supplement for improving intestinal epithelial barrier dysfunction.
引用
收藏
页数:9
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