Glutamine protects intestine against ischemia-reperfusion injury by alleviating endoplasmic reticulum stress induced apoptosis in rats
Acta cir. bras
; 35(1): e202000104, 2020. graf
Article
in En
| LILACS
| ID: biblio-1088525
Responsible library:
BR1.1
ABSTRACT
Abstract Purpose Glutamine, as an essential part of enteral nutrition and parenteral nutrition agent, has been widely recognized to be a kind of important intestinal mucosa protectant in clinical practice and experimental research. However, the mechanisms of its protective effects are still not fully understand. Consequently, this study aimed to explore the potential mechanism of glutamine on ischemia-reperfusion (I/R) injury induced endoplasmic reticulum (ER) stress in intestine. Methods An experimental model of intestinal I/R in rats was established by 1 hour occlusion of the superior mesenteric artery followed by 3 hours of reperfusion. Morphologic changes of intestinal mucosa, apoptosis of epithelial cells, and expression of intestinal Grp78, Gadd153, Caspase-12, ATF4, PERK phosphorylation (P-PERK) and elF2αphosphorylation(P-elF2α) were determined. Results After I/R, the apoptotic index of intestinal mucosa epithelial cells observably increased with notable necrosis of intestinal mucosa, and the expressions of Grp78, Gadd153, Caspase-12, ATF4, P-PERK and P-elF2αall were increased. However, treatment with glutamine could significantly relieve intestinal I/R injury and apoptosis index. Moreover, glutamine could clearly up-regulate the expression of Grp78, restrain P-PERK and P-elF2α, and reduce ATF4, Gadd153 and Caspase-12 expressions. Conclusion Glutamine may be involved in alleviating ER stress induced intestinal mucosa cells apoptosis.
Key words
Full text:
1
Index:
LILACS
Main subject:
Reperfusion Injury
/
Apoptosis
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Protective Agents
/
Endoplasmic Reticulum Stress
/
Glutamine
/
Intestinal Mucosa
Type of study:
Prognostic_studies
Limits:
Animals
Language:
En
Journal:
Acta cir. bras
Journal subject:
CIRURGIA GERAL
/
Procedimentos Cir£rgicos Operat¢rios
Year:
2020
Type:
Article