scholarly journals Research progress on the protective effects of fucoidan against intestinal mucosal barrier dysfunction (Review)

2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Xia Qiu ◽  
Fahe Wang ◽  
Yimin Qin ◽  
Zhanyi Sun ◽  
Peili Shen
Keyword(s):  
Research Progress ◽  
Mucosal Barrier ◽  
Protective Effects ◽  
Barrier Dysfunction ◽  
Intestinal Mucosal Barrier

scholarly journals Research progress on gut health of farmers teleost fish: a viewpoint concerning the intestinal mucosal barrier and the impact of its damage

2020 ◽  
Vol 30 (4) ◽  
pp. 569-586
Author(s):  
Hongling Zhang ◽  
Chao Ran ◽  
Tsegay Teame ◽  
Qianwen Ding ◽  
Seyed Hossein Hoseinifar ◽  
...  
Keyword(s):  
Teleost Fish ◽  
Research Progress ◽  
Mucosal Barrier ◽  
Gut Health ◽  
Intestinal Mucosal Barrier ◽  
The Impact

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.

scholarly journals N-Acetyl Serotonin Alleviates Oxidative Damage by Activating Nuclear Factor Erythroid 2-Related Factor 2 Signaling in Porcine Enterocytes

Antioxidants ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 303
Author(s):  
Haiwei Liang ◽  
Ning Liu ◽  
Renjie Wang ◽  
Yunchang Zhang ◽  
Jingqing Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gastrointestinal Diseases ◽  
Mucosal Barrier ◽  
Related Factor ◽  
Protective Effects ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Downstream Target ◽  
Underlying Mechanisms ◽  
And Function

Apoptosis of intestinal epithelial cells following oxidative stress is a major cause of mucosal barrier dysfunction and is associated with the pathogenesis of various gastrointestinal diseases. Although L-tryptophan (Trp) is known to improve intestinal integrity and function, a beneficial effect of N-acetyl serotonin (NAS), a metabolite of Trp, on the apoptosis of enterocytes and the underlying mechanisms remain largely unknown. In the present study, we showed that porcine enterocytes treated with 4-hydroxy-2-nonenal (4-HNE), a metabolite of lipid peroxidation, led to upregulation of apoptotic proteins, including Bax and cleaved caspase-3, and reduction of tight junction proteins. These effects of 4-HNE were significantly abrogated by NAS. In addition, NAS reduced ROS accumulation while increasing the intracellular concentration of glutathione (GSH), and the abundance of the Nrf2 protein in the nucleus and its downstream target proteins. Importantly, these protective effects of NAS were abrogated by Atra, an inhibitor of Nrf2, indicating a dependence on Nrf2 signaling. Taken together, we demonstrated that NAS attenuated oxidative stress-induced cellular injury in porcine enterocytes by regulating Nrf2 signaling. These findings provide new insights into a functional role of NAS in maintaining intestinal homeostasis.

scholarly journals Simvastatin Ameliorates PAK4 Inhibitor-Induced Gut and Lung Injury

2017 ◽  
Vol 2017 ◽  
pp. 1-9
Author(s):  
Shuming Pan ◽  
Zengbin Wu ◽  
Xuan Liu ◽  
Jiameng Chen ◽  
Huiqi Wang ◽  
...  
Keyword(s):  
Lung Injury ◽  
Mitogen Activated Protein Kinase ◽  
Mucosal Barrier ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Intestinal Mucosal Barrier ◽  
Protein Levels ◽  
Mitogen Activated Protein ◽  
P21 Activated Kinase ◽  
D Values

P21 activated kinase 4 (PAK4), a key regulator of cytoskeletal rearrangement and endothelial microparticles (EMPs), is released after lipopolysaccharide (LPS) stimulation. In addition, it participates in LPS-induced lung injury. In this study, forty-eight Sprague Dawley (SD) rats were divided into two groups, including PAK4 inhibitor (P) and PAK4 inhibitor + simvastatin (P + S) treatment groups. All rats were given PAK4 inhibitor (15 mg/kg/d) orally. Immediately after PAK4 inhibitor administration, simvastatin was injected intraperitoneally to P + S group animals at 20 mg/kg/day. Then, treatment effects on the intestinal mucosal barrier and lung injury caused by PAK4 inhibitor and simvastatin were assessed. The results showed that gut Zonula Occludens- (ZO-) 1, PAK4, mitogen-activated protein kinase 4 (MPAK4), and CD11c protein levels were reduced, while plasma endotoxin levels were increased after administration of PAK4 inhibitor. Furthermore, compared with normal rats, wet-to-dry (W/D) values of lung tissues and circulating EMP levels were increased in the treatment group, while PAK4 and CD11c protein amounts were reduced. Therefore, in this lung injury process induced by PAK4 inhibitor, the protective effects of simvastatin were reflected by intestinal mucosal barrier protection, inflammatory response regulation via CD11c+ cells, and cytoskeleton stabilization. In summary, PAK4 is a key regulator in the pathophysiological process of acute lung injury (ALI) and can be a useful target for ALI treatment.

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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