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Updated: Oct 1, 2026
Murine Model of Intestinal Ischemia-reperfusion Injury
Published on: May 11, 2016
Protective effect of glutamine on the main and adjacent organs damaged by ischemia-reperfusion in rats
Renata Minuzzo Hartmann1,2,3, Francielli Licks4,2,3, Elizângela Gonçalves Schemitt1,2,3
1Graduate Program in Medicine: Medical Sciences, Universidade Federal do Rio Grande do Sul - UFRGS, Porto Alegre, Rio Grande do Sul, Brazil.
Abstract:
Intestinal ischemia and reperfusion (I/R) causes cellular and tissue damage to the intestine and remote organs such as the liver. Increased production of ROS and nitric oxide and dysregulation of cytoprotective enzymes may be involved in intestinal I/R. The aim was to evaluate the protective effects of glutamine on the intestine and liver of rats with intestinal I/R injury. Twenty male Wistar rats (300 g) were divided into four groups: sham-operated (SO), glutamine + SO (G + SO), I/R, and glutamine + I/R (G + I/R). Occlusion of the SMA for 30 min was followed by 15-min reperfusion. Glutamine (25 mg/kg/day) was administered once daily 24 and 48 h before I/R induction. Blood and tissue of were collected for aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, histopathological analysis, immunohistochemistry of IL-1β and TNF-α, thiobarbituric acid reactive substance (TBARS) and nitric oxide, Nrf2/keap1, superoxide dismutase (SOD), NADPH quinone oxidoreductase1 (NQO1), inducible nitric oxide synthase (iNOS), heat shock protein (HSP70), glucose-regulated protein 78 (GRP78), and activating transcription factor 6 (ATF-6) by western blot. Statistic analysis by ANOVA-Student-Newman-Keuls test (mean ± SE) significantly was p < 0.05. Tissue damage, AST, ALT, IL-1β, TNF-α, TBARS, NO, Keap1, iNOS, GRP78, and ATF-6 expression were significantly lower in the G + I/R group as compared to the I/R group. Expression of Nrf2, SOD, NQO1, and HSP70, was significantly higher in the G + I/R group as compared to I/R group. Pre-treatment with glutamine provided protection against oxidative damage in the intestine and liver in an experimental model of intestinal I/R.
Insights
Glutamine supplementation protected rats against intestinal ischemia and reperfusion (I/R) injury. It reduced tissue damage and oxidative stress markers in the intestine and liver, highlighting glutamine
Area of Science:
- Gastroenterology
- Cellular and Molecular Medicine
- Surgical Research
Background:
- Intestinal ischemia and reperfusion (I/R) causes significant tissue damage to the intestine and remote organs like the liver.
- Oxidative stress, involving reactive oxygen species (ROS) and nitric oxide, along with altered cytoprotective enzyme activity, contributes to I/R injury.
- Understanding protective mechanisms is crucial for mitigating I/R-induced organ damage.
Purpose of the Study:
- To investigate the protective effects of glutamine pre-treatment on intestinal and liver tissues subjected to I/R injury in a rat model.
- To evaluate the impact of glutamine on oxidative stress markers, inflammatory responses, and key protein expressions related to cellular protection.
Main Methods:
- Twenty male Wistar rats were divided into four groups: sham-operated (SO), glutamine + SO (G+SO), I/R, and glutamine + I/R (G+I/R).
- Intestinal I/R was induced by 30 minutes of superior mesenteric artery (SMA) occlusion followed by 15 minutes of reperfusion.
- Glutamine (25 mg/kg/day) was administered 24 and 48 hours pre-injury. Blood and tissue samples were analyzed for biochemical markers, histopathology, and protein expression (e.g., IL-1β, TNF-α, Nrf2, SOD, HSP70) via Western blot.
Main Results:
- Glutamine pre-treatment significantly reduced tissue damage, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and markers of oxidative stress (TBARS, nitric oxide) in the G+I/R group compared to the I/R group.
- Expression of pro-inflammatory cytokines (IL-1β, TNF-α) and endoplasmic reticulum stress markers (GRP78, ATF-6) were significantly lower in the G+I/R group.
- Conversely, the expression of the antioxidant transcription factor Nrf2 and cytoprotective enzymes (SOD, NQO1) and heat shock protein (HSP70) was significantly upregulated in the G+I/R group.
Conclusions:
- Pre-treatment with glutamine demonstrates significant protective effects against intestinal and liver injury induced by I/R in rats.
- Glutamine mitigates I/R-induced damage by reducing oxidative stress, inflammation, and endoplasmic reticulum stress, while enhancing the Nrf2-mediated antioxidant response.
- These findings suggest glutamine as a potential therapeutic agent for preventing or treating I/R injury in clinical settings.
