scholarly journals Sodium Decanoate Improves Intestinal Epithelial Barrier and Antioxidation via Activating G Protein-Coupled Receptor-43

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2756
Author(s):  
Jinbiao Zhao ◽  
Jinhua Hu ◽  
Xi Ma
Keyword(s):  
Antioxidant Capacity ◽  
G Protein ◽  
Sodium Butyrate ◽  
Intestinal Barrier ◽  
Intestinal Morphology ◽  
Intestinal Epithelial ◽  
G Protein Coupled Receptor ◽  
Α Diversity ◽  
Sodium Decanoate ◽  
G Protein Coupled

The study was conducted to explore actions of decanoic acid on regulating intestinal barrier and antioxidant functions in intestinal epithelium cells isolated from porcine jejunum (IPEC-J2) and C57/BL6 mice models. In vitro and vivo assays, mice and IPEC-J2 cells treated by H2O2 were disposed of sodium decanoate and sodium butyrate to determine intestinal barrier and antioxidant functions of the host. Results showed that sodium decanoate upregulated expression of tight junction proteins and improved antioxidant capacity in both IPEC-J2 cells treated by H2O2 and mice models (p < 0.05). Sodium decanoate increased weight gain and ileal villus height of mice compared with control and sodium butyrate treatments (p < 0.05). Sodium decanoate increased α-diversity of ileal microbiota, volatile fatty acids concentration, and G protein-coupled receptor-43 (GPR-43) expression in the ileum and colon of mice (p < 0.05). In conclusion, sodium decanoate improved antioxidant capacity, intestinal morphology, and gut physical barrier of intestinal epithelial cells, resulting in an increase growth performance of mice, which is mediated through activating GPR-43 signaling.

scholarly journals G Protein-Coupled Receptor 109A Maintains the Intestinal Integrity and Protects Against ETEC Mucosal Infection by Promoting IgA Secretion

2021 ◽  
Vol 11 ◽  
Author(s):  
Yuhong Gong ◽  
Xinxin Jin ◽  
Boyu Yuan ◽  
Yantao Lv ◽  
Guangmou Yan ◽  
...  
Keyword(s):  
Tight Junction ◽  
G Protein ◽  
Sodium Butyrate ◽  
Intestinal Tract ◽  
Intestinal Barrier ◽  
Tight Junction Proteins ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled ◽  
Etec Infection ◽  
Junction Proteins

Several studies have reported an intricate link between the G protein-coupled receptor 109A (GPR109A) and intestinal health. Upon activation, induced by butyric acid and β-hydroxybutyric acid, GPR109A regulates the expression of tight junction proteins, exerts anti-inflammatory effects, and maintains the integrity of the intestinal barrier. However, its function and the mechanism of action in combating the infection caused by exogenous pathogenic microorganisms remain unclear. This study established an animal model of infection by oral enterotoxigenic Escherichia coli (ETEC) gavage to examine the underlying mechanism(s) and protective effects of GPR109A on the intestinal tract. Experimental GPR109A–/–and GPR109A+/+ mice were orally administered with 1 × 109 colony-forming units (CFUs) of ETEC, and changes in body weight were then observed. The colonization and translocation of ETEC in the intestine were detected by the plate counting method. The expression of tight junction proteins and the levels of inflammatory factors and secretory IgA (SIgA) in the intestine were detected by quantitative real-time polymerase chain reaction (q-PCR), western blotting, enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry. The results demonstrated that GPR109A–/–mice were more susceptible to ETEC infection, showing more severe inflammatory reactions and intestinal damage. Moreover, the secretion of IgA in the intestinal tract of GPR109A+/+ mice was significantly increased after ETEC infection, whereas the IgA levels in GPR109A–/–mice did not change significantly. We added 5 g/L sodium butyrate to the drinking water of all mice. The GPR109A+/+ mice were protected against ETEC infection and no effect was observed in GPR109A–/–mice. Similarly, sodium butyrate increased the SIgA content in the gut of the GPR109A+/+ mice and no effect was observed in GPR109A–/–mice. In conclusion, activated GPR109A is effective against the colonization and translocation of ETEC in the gut and maintains the integrity of the intestinal barrier, possibly by promoting the secretion of intestinal IgA.

Involvement of G protein-coupled receptor kinase 4 and 6 in rapid desensitization of dopamine D1 receptor in rat IEC-6 intestinal epithelial cells

2004 ◽  
Vol 287 (4) ◽  
pp. R772-R779 ◽  
Author(s):  
Sónia Fraga ◽  
Pedro A. Jose ◽  
Patrício Soares-da-Silva
Keyword(s):  
G Protein ◽  
D1 Receptor ◽  
Skf 38393 ◽  
Epithelial Cell Line ◽  
Intestinal Epithelial ◽  
Receptor Kinase ◽  
G Protein Coupled Receptor ◽  
Dependent Inhibition ◽  
G Protein Coupled ◽  
Stimulation Of

Dopamine-induced inhibition of Na+-K+-ATPase has been suggested to play a role in the regulation of Na+ absorption at the intestinal level, and these effects were mediated by dopamine D1-like receptors. The aim of this work was to evaluate the effect of the activation of the D1-like receptors on the activity of the Na+/H+ exchanger (NHE) in the rat intestinal epithelial cell line IEC-6. The presence of D1 receptors was confirmed by immunoblotting. The dopamine D1-like receptor agonist SKF-38393 produced a concentration-dependent inhibition of NHE activity and stimulation of adenylyl cyclase (AC), this being antagonized by the D1 selective antagonist SKF-83566. Effects of SKF-38393 on NHE and AC activities were maximal at 5 min of exposure to the agonist and rapidly diminished with no effect at 25 min. Exposure of cells for 25 min to dibutyryl-cAMP (0.5 mM) or to the AC activator forskolin (3 μM) effectively inhibited NHE activity. Pretreatment of cells with heparin (1 μM), a nonselective G protein-coupled receptor kinase (GRK) inhibitor, prevented the loss of effects on NHE activity after 25 min exposure to SKF-38393. The presence of GRK4, GRK6A, and GRK6B was confirmed by immunoblotting. Overnight treatment with the anti-GRK4–6 antibody complexed with Lipofectin was also effective in preventing loss of the effects of SKF-38393 on NHE and AC activities. It is concluded that dopamine D1 receptors in IEC-6 rapidly desensitize to D1-like agonist stimulation and GRK4 and 6 appear to be involved in agonist-mediated responsiveness and desensitization.

Tu1351 Functional Consequences of G Protein-Coupled Receptor 68 (GPR68/OGR1) Overexpression in Intestinal Epithelial Cells

2012 ◽  
Vol 142 (5) ◽  
pp. S-809
Author(s):  
Cheryl de Valliere ◽  
Solange Vidal ◽  
Jyrki J. Eloranta ◽  
Silvia Lang ◽  
Irina Vetter ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
G Protein ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
G Protein Coupled Receptor ◽  
Functional Consequences ◽  
G Protein Coupled
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