Early weaning increases intestinal permeability, alters expression of cytokine and tight junction proteins, and activates mitogen-activated protein kinases in pigs1

2013 ◽  
Vol 91 (3) ◽  
pp. 1094-1101 ◽  
Author(s):  
C. H. Hu ◽  
K. Xiao ◽  
Z. S. Luan ◽  
J. Song
Keyword(s):  
Tight Junction ◽  
Protein Kinases ◽  
Intestinal Permeability ◽  
Tight Junction Proteins ◽  
Early Weaning ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein ◽  
Junction Proteins

scholarly journals Niacin and Butyrate: Nutraceuticals Targeting Dysbiosis and Intestinal Permeability in Parkinson’s Disease

Nutrients ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 28
Author(s):  
Tennekoon B. Karunaratne ◽  
Chijioke Okereke ◽  
Marissa Seamon ◽  
Sharad Purohit ◽  
Chandramohan Wakade ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Tight Junction ◽  
G Protein ◽  
Intestinal Permeability ◽  
Macrophage Polarization ◽  
Tight Junction Proteins ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled ◽  
Junction Proteins

Dysbiosis is implicated by many studies in the pathogenesis of Parkinson’s disease (PD). Advances in sequencing technology and computing have resulted in confounding data regarding pathogenic bacterial profiles in conditions such as PD. Changes in the microbiome with reductions in short-chain fatty acid (SCFA)-producing bacteria and increases in endotoxin-producing bacteria likely contribute to the pathogenesis of PD. GPR109A, a G-protein coupled receptor found on the surface of the intestinal epithelium and immune cells, plays a key role in controlling intestinal permeability and the inflammatory cascade. The absence of GPR109A receptors is associated with decreased concentration of tight junction proteins, leading to increased intestinal permeability and susceptibility to inflammation. In inflammatory states, butyrate acts via GPR109A to increase concentrations of tight junction proteins and improve intestinal permeability. Niacin deficiency is exacerbated in PD by dopaminergic medications. Niacin supplementation has been shown to shift macrophage polarization from pro-inflammatory to an anti-inflammatory profile. Niacin and butyrate, promising nutrients and unique ligands for the G protein-coupled receptor GPR109A, are reviewed in this paper in detail.

scholarly journals Dexmedetomidine protects against burn-induced intestinal barrier injury via the MLCK/p-MLC signalling pathway

2020 ◽  
Author(s):  
Chao Qin ◽  
Yi Jiang ◽  
Xing Chen ◽  
Yingxue Bian ◽  
Yaoqi Wang ◽  
...  
Keyword(s):  
Tight Junction ◽  
Intestinal Permeability ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Burn Injury ◽  
Intestinal Barrier ◽  
Signalling Pathway ◽  
Tight Junction Proteins ◽  
Anti Inflammatory ◽  
Junction Proteins

Abstract Background Dexmedetomidine, a potent α2-adrenoceptor agonist with analgesic, sedative, anti-inflammatory, and anti-apoptotic effects, is commonly used in patients with critical illness in intensive care units. Accumulating evidence indicates that dexmedetomidine can protect against intestinal dysfunction. However, the specific mechanisms of its protective effects against burn-induced intestinal barrier injury remain unclear. Here, we aimed to explore the possible positive effects of dexmedetomidine on burn-induced intestinal barrier injury and the role of the myosin light chain kinase (MLCK)/phosphorylated myosin light chain (p-MLC) signalling pathway in an experimental model of burn injury.Methods In this study, the intestinal permeability of burn-induced intestinal barrier damage was assessed by estimating the plasma concentration of 4.4 kDa fluorescein isothiocyanate-labelled dextran (FITC-dextran). Histological changes were evaluated using haematoxylin and eosin (HE) staining. Tight junction proteins were evaluated by western blot and immunofluorescence analyses to assess the structural integrity of intestinal tight junctions. The level of inflammation was determined by enzyme-linked immunosorbent assay (ELISA).Results Our findings demonstrated that the increase in intestinal permeability caused by burn injury is accompanied by histological damage to the intestine, decreases in the expression of the tight junction proteins Zonula Occludens-1 (ZO-1) and Occludin, increases in inflammatory cytokine levels and elevation of both MLCK protein expression and MLC phosphorylation. After dexmedetomidine treatment, the burn-induced changes were ameliorated.Conclusions In conclusion, dexmedetomidine exerted an anti‑inflammatory effect and protected tight junction complexes against burn‑induced intestinal barrier damage by inhibiting the MLCK/p-MLC signalling pathways, suggesting that it may be an effective drug in the treatment of burn-induced intestinal injury.Trial registration Not appliance.

Sign in / Sign up

Export Citation Format

Share Document