scholarly journals Resveratrol alleviates intestinal mucosal barrier dysfunction in dextran sulfate sodium-induced colitis mice by enhancing autophagy

2020 ◽  
Vol 26 (33) ◽  
pp. 4945-4959
Author(s):  
Hang-Hai Pan ◽  
Xin-Xin Zhou ◽  
Ying-Yu Ma ◽  
Wen-Sheng Pan ◽  
Fei Zhao ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Mucosal Barrier ◽  
Barrier Dysfunction ◽  
Intestinal Mucosal Barrier

Gut relief formula attenuates dextran sulfate sodium-induced colitis by regulating NF-κB signaling and the intestinal microbiota in mice

2021 ◽  
Author(s):  
Xuemeng Si ◽  
Ning Liu ◽  
Hai Jia ◽  
Jiaqi Wang ◽  
Lina Pan ◽  
...  
Keyword(s):  
Intestinal Microbiota ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Mucosal Barrier ◽  
Mucosal Inflammation ◽  
Barrier Dysfunction

Gut relief formula administration alleviated mucosal inflammation and mucosal barrier dysfunction by inhibiting STAT3 and NF-κB activity and upregulating abundances of Lactobacillus in DSS-induced colitis.

scholarly journals SLC26A3 (DRA) prevents TNF-alpha-induced barrier dysfunction and dextran sulfate sodium-induced acute colitis

2018 ◽  
Vol 98 (4) ◽  
pp. 462-476 ◽  
Author(s):  
Xiangming Ding ◽  
Dongxiao Li ◽  
Mengke Li ◽  
Han Wang ◽  
Qin He ◽  
...  
Keyword(s):  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Tnf Alpha ◽  
Barrier Dysfunction ◽  
Acute Colitis

scholarly journals Probiotic Mixture Protects Dextran Sulfate Sodium-Induced Colitis by Altering Tight Junction Protein Expressions and Increasing Tregs

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Yingdi Zhang ◽  
Xiaojing Zhao ◽  
Yunjuan Zhu ◽  
Jingjing Ma ◽  
Haiqin Ma ◽  
...  
Keyword(s):  
Tight Junction ◽  
Peripheral Blood ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Intestinal Inflammation ◽  
Experimental Colitis ◽  
Mucosal Barrier ◽  
Intestinal Damage ◽  
Protective Effects ◽  
Junction Protein

Bifico is a probiotic mixture containing Bifidobacterium, Lactobacillus acidophilus, and Enterococcus. Studies support that Bifico has a protective effect in experimental colitis (IL-10-deficient and TNBS) models and in patients with inflammatory bowel disease (IBD). However, the mechanism underlying the protective effects of this mixture of probiotic bacteria remains incompletely clear. Here, we investigated the effect of Bifico on intestinal inflammation. In an in vivo experiment, dextran sulfate sodium was used to induce colitis. Bifico treatment significantly attenuated the severity of colitis in this model. Bifico increased the expression of tight junction proteins (TJs). In addition, Bifico increased the number of Tregs, but reduced the number of total CD4+ T cells in the peripheral blood. Furthermore, the expression of colonic CD4 protein was decreased while the level of forkhead box P3 (Foxp3) was upregulated. These results suggested that Bifico exerts beneficial effects on experimental colitis by increasing the expressions of TJs, upregulating the number of Tregs, and reducing the total CD4+ T cell number in both colon and peripheral blood. The intestinal damage in the pretreated + treated-Bifico-colitis group was more severe than that in only the pretreated-Bifico-colitis group. This suggested that Bifico might aggravate intestinal damage when the mucosal barrier is impaired.

Intestinal mucosal barrier dysfunction in SAP patients with MODS ameliorated by continuous blood purification

2017 ◽  
Vol 41 (1) ◽  
pp. 43-51
Author(s):  
Qing Shen ◽  
Zhengrong Li ◽  
Shanshan Huang ◽  
Liman Li ◽  
Hua Gan ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Mucosal Barrier ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Intestinal Mucosal Barrier ◽  
Epithelial Monolayer ◽  
Tnf Α ◽  
Monolayer Permeability ◽  
Α Level ◽  
Junction Proteins

Background: Dysfunction of the intestinal mucosal barrier plays an important role in the pathophysiology of severe acute pancreatitis (SAP). Continuous blood purification (CBP) has been shown to improve the prognosis of SAP patients. In order to investigate the effect of CBP on intestinal mucosal barrier dysfunction in SAP patients with MODS, we conducted in vivo and in vitro experiments to explore the underlying mechanisms. Methods: The markers for the assessment of intestinal mucosal barrier function including serum diamine oxidase (DAO), endotoxin and intestinal epithelial monolayer permeability were detected during CBP therapy. The distribution and expression of cytoskeleton protein F-actin and tight junction proteins claudin-1 were observed. In addition, Rho kinase (ROCK) mRNA expression and serum tumor necrosis factor-alpha (TNF-α) levels during CBP were determined. Results: SAP patients with MODS had increased levels of serum DAO, endotoxin and intestinal epithelial monolayer permeability when compared with normal controls. While the distribution of F-actin and claudin-1 was rearranged, and the expression of claudin-1 significantly decreased, but F-actin had no change. Meanwhile, ROCK mRNA expression and serum TNF-α level were increased. However, after CBP treatment, levels of serum DAO, endotoxin and intestinal epithelial monolayer permeability decreased. The F-actin and claudin-1 reorganization attenuated and the expression of claudin-1 increased. At the same time, ROCK mRNA expression and serum TNF-α level were decreased. Conclusions: CBP can effectively improve intestinal mucosal barrier dysfunction. The beneficial effect is associated with the improvement of cytoskeleton and tight junction proteins in stability by downregulation of ROCK mRNA expression through the removal of excess proinflammatory factors.

Bronchoscopy induces intestinal mucosal barrier dysfunction: a possible role for nitric oxide

2003 ◽  
Vol 67 (9) ◽  
pp. 957-963 ◽  
Author(s):  
Ali Nayci ◽  
Sibel Atis ◽  
Derya Umit Talas ◽  
Ayse Polat ◽  
Ozlen Bagdatoglu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mucosal Barrier ◽  
Barrier Dysfunction ◽  
Intestinal Mucosal Barrier

scholarly journals Intestinal Mucosal Barrier Is Injured by BMP2/4 via Activation of NF-κB Signals after Ischemic Reperfusion

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Kang Chen ◽  
Wei Xie ◽  
Binyu Luo ◽  
Weidong Xiao ◽  
Daniel H. Teitelbaum ◽  
...  
Keyword(s):  
Receptor Expression ◽  
Mucosal Barrier ◽  
Inflammatory Factors ◽  
Pyrrolidine Dithiocarbamate ◽  
Barrier Dysfunction ◽  
Intestinal Mucosal Barrier ◽  
Ischemic Reperfusion ◽  
Junction Protein ◽  
Type Ia

Intestinal ischemic reperfusion (I/R) can cause dysfunction of the intestinal mucosal barrier; however, the mechanism of the intestinal mucosal barrier dysfunction caused by I/R remains unclear. In this study, using intestinal epithelial cells under anaerobic cultivation and an in vivo rat intestinal I/R model, we found that hypoxia and I/R increased the expression of BMP2/4 and upregulated BMP type Ia receptor and BMP type II receptor expression. We also found that exogenous BMP2/4 can activate the ERK and AKT signaling pathways in rat small intestine (IEC-6) cells, thereby activating NF-κB signaling, which leads to increased levels of inflammatory factors, such as TNF-αand IL-6. Furthermore, recombinant BMP2/4 decreased the expression of the tight junction protein occludin via the activation of the NF-κB pathway; these effects were abolished by treatment with the BMP-specific antagonist noggin or the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC). All these factors can destroy the intestinal mucosal barrier, thereby leading to weaker barrier function. On the basis of these data, we conclude that BMP2/4 may act as the pathogenic basis for intestinal mucosal barrier dysfunction when the intestines suffer an I/R injury. Our results provide background for the development pharmacologic interventions in the management of I/R injury.

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