MicroRNA‐21 increases the expression level of occludin through regulating ROCK1 in prevention of intestinal barrier dysfunction

2018 ◽  
Vol 120 (3) ◽  
pp. 4545-4554 ◽  
Author(s):  
Zhihua Liu ◽  
Chao Li ◽  
Shihua Chen ◽  
Hongcheng Lin ◽  
Huan Zhao ◽  
...  
2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Zeyang Chen ◽  
Jianqiang Tang ◽  
Pengyuan Wang ◽  
Jing Zhu ◽  
Yucun Liu

Objectives. Substantial studies have demonstrated that an elevated concentration of deoxycholic acid (DCA) in the colonic lumen may play a critical role in the pathogenesis of intestinal barrier dysfunction and inflammatory bowel disease (IBD). The purpose of this study was to investigate the protective effects of GYY4137, as a novel and synthetic H2S donor, on the injury of intestinal barrier induced by sodium deoxycholate (SDC) both in vivo and in vitro. Methods. In this study, Caco-2 monolayers and mouse models with high SDC concentration in the lumen were used to study the effect of GYY4137 on intestinal barrier dysfunction induced by SDC and its underlying mechanisms. Results. In Caco-2 monolayers, a short period of addition of SDC increased the permeability of monolayers obviously, changed distribution of tight junctions (TJs), and improved the phosphorylation level of myosin light chain kinase (MLCK) and myosin light chain (MLC). However, pretreatment with GYY4137 markedly ameliorated the SDC-induced barrier dysfunction. Being injected with GYY4137 could enable mice to resist the SDC-induced injury of the intestinal barrier. Besides, GYY4137 promoted the recovery of the body weight and intestinal barrier histological score of mice with the gavage of SDC. GYY4137 also attenuated the decreased expression level of TJs in mice treated with SDC. Conclusion. Taken together, this research suggests that GYY4137 preserves the intestinal barrier from SDC-induced injury via suppressing the activation of P-MLCK-P-MLC2 signaling pathway and increasing the expression level of tight junctions.


2006 ◽  
Vol 51 (9) ◽  
pp. 1549-1556 ◽  
Author(s):  
Desheng Song ◽  
Bin Shi ◽  
Hua Xue ◽  
Yousheng Li ◽  
Xiaodong Yang ◽  
...  

2006 ◽  
Vol 41 (8) ◽  
pp. 1386-1391 ◽  
Author(s):  
Ali Nayci ◽  
Sibel Atis ◽  
Gulden Ersoz ◽  
Ayse Polat ◽  
Derya Talas

Amino Acids ◽  
2021 ◽  
Author(s):  
Tatsuya Hasegawa ◽  
Ami Mizugaki ◽  
Yoshiko Inoue ◽  
Hiroyuki Kato ◽  
Hitoshi Murakami

AbstractIntestinal oxidative stress produces pro-inflammatory cytokines, which increase tight junction (TJ) permeability, leading to intestinal and systemic inflammation. Cystine (Cys2) is a substrate of glutathione (GSH) and inhibits inflammation, however, it is unclear whether Cys2 locally improves intestinal barrier dysfunction. Thus, we investigated the local effects of Cys2 on oxidative stress-induced TJ permeability and intestinal inflammatory responses. Caco-2 cells were cultured in a Cys2-supplemented medium for 24 h and then treated with H2O2 for 2 h. We assessed TJ permeability by measuring transepithelial electrical resistance and the paracellular flux of fluorescein isothiocyanate–dextran 4 kDa. We measured the concentration of Cys2 and GSH after Cys2 pretreatment. The mRNA expression of pro-inflammatory cytokines was assessed. In addition, the levels of TJ proteins were assessed by measuring the expression of TJ proteins in the whole cells and the ratio of TJ proteins in the detergent-insoluble fractions to soluble fractions (IS/S ratio). Cys2 treatment reduced H2O2-induced TJ permeability. Cys2 did not change the expression of TJ proteins in the whole cells, however, suppressed the IS/S ratio of claudin-4. Intercellular levels of Cys2 and GSH significantly increased in cells treated with Cys2. Cys2 treatment suppressed the mRNA expression of pro-inflammatory cytokines, and the mRNA levels were significantly correlated with TJ permeability. In conclusion, Cys2 treatment locally reduced oxidative stress-induced intestinal barrier dysfunction possively due to the mitigation of claudin-4 dislocalization. Furthermore, the effect of Cys2 on the improvement of intestinal barrier function is related to the local suppression of oxidative stress-induced pro-inflammatory responses.


2021 ◽  
Author(s):  
Fangfang Yan ◽  
Wanbing Chen ◽  
Li Zhao ◽  
Qun Lu ◽  
Chengming Wang ◽  
...  

Procyanidins can alleviate small intestine damage induced by acrylamide (ACR). However, little is known about whether procyanidins after gastrointestinal digestion can prevent ACR-induced intestinal barrier damage and the possible mechanism....


2019 ◽  
Vol 10 (10) ◽  
pp. 6517-6532 ◽  
Author(s):  
Hang Xu ◽  
Chunfang Zhao ◽  
Yutian Li ◽  
Ruiyu Liu ◽  
Mingzhang Ao ◽  
...  

Pyracantha fortuneana fruit extract (PFE) exhibits beneficial effects on IBF in association with the modulation of glycolipid digestion and gut microbiota in HFD-fed obese rats.


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