Effect of glutamine on liver injuries induced by intestinal ischemia-reperfusion in rats
Intestinal ischemia-reperfusion (I/R) injury may cause cell and tissue damage, reaching also other organs such as the liver. Because of the involvement of free radicals in I/R injury, treatment options with antioxidants have been studied and tested. To evaluate the effect of glutamine (Gln) in the l...
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Published in | Nutrición hospitalaria : organo oficial de la Sociedad Española de Nutrición Parenteral y Enteral Vol. 34; no. 3; pp. 548 - 554 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Spain
Grupo Arán
05.06.2017
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Subjects | |
Online Access | Get full text |
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Summary: | Intestinal ischemia-reperfusion (I/R) injury may cause cell and tissue damage, reaching also other organs such as the liver. Because of the involvement of free radicals in I/R injury, treatment options with antioxidants have been studied and tested.
To evaluate the effect of glutamine (Gln) in the liver of animals with intestinal I/R injury.
We used 20 male Wistar rats divided into four groups: sham-operated (SO); glutamine + sham-operated (G+SO); intestinal ischemia-reperfusion (I/R); glutamine + intestinal ischemia-reperfusion (G+I/R). The superior mesenteric artery was clamped for 30 minutes and reperfused for 15 minutes. Gln (25 mg/kg/day) diluted in 1 ml of saline was administered intraperitoneally on the two days before I/R induction.
Levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP), lipid peroxidation (LPO) and expressions of interleukin-6 (IL-6) and nuclear factor kappa B (NF-kB) showed a significant reduction in the G+I/R group as compared with the I/R group. The activity of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and the levels of glutathione (GSH) showed an increase in the G+I/R group as compared with the I/R group.
Pretreatment with Gln reduced oxidative, tissue damage and showed a decrease expression of inflammatory mediators. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0212-1611 1699-5198 1699-5198 |
DOI: | 10.20960/nh.643 |