Effects of L-alanyl-glutamine upon the blood and kidney biochemical parameters in the rat hind limb model of ischemia/reperfusion

Alves, Marcos Antônio; Guimarães, Sérgio Botelho; Dias, Daniel Aguiar; Vasconcelos, Paulo Roberto Cavalcante de; Coelho, Vicente de Paulo Martins; Vasconcelos, Paulo Roberto Leitão de

doi:10.1590/s0102-86502005000600009

Cited by 12 publications

(8 citation statements)

References 11 publications

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“…Gln is an important precursor of adenosine triphosphate and adenosine monophosphate which are used to power the intestinal mucosal cell metabolic oxidation (11,12). Furthermore, Gln is the precursor to glutathione, an important antioxidant that protects intestinal epithelial cells from oxidant damage and inhibits intestinal mucosal apoptosis (13,14).…”

Section: Discussionmentioning

confidence: 99%

Glutamine decreases intestinal mucosal injury in a rat model of intestinal ischemia-reperfusion by downregulating HMGB1 and inflammatory cytokine expression

Xiao-liang

Zhang

Wang

et al. 2016

Experimental and Therapeutic Medicine

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Abstract.Intestinal ischemia-reperfusion (IR) is a common clinical pathophysiological process that is common in severe trauma, major surgery, and in post-resuscitation. Glutamine (Gln) reduces intestinal IR injury, however, its mechanism of action remains to be determined. High mobility group box 1 (HMGB1) protein, nuclear factor-κB (NF-κB), tumor necrosis factor-α (TNF-α), and interleukin-1 (IL-1) are mediators involved in the pathophysiology of intestinal IR injury. The aim of the present study was to investigate the effects of Gln on the intestinal mucosa of HMGB1 expression following IR to determine whether Gln relieved intestinal IR injury in the intestinal mucosal barrier. Forty-eight Sprague-Dawley rats were included in the present study. A model of intestinal ischemia-reperfusion injury was established by clamping the superior mesenteric artery of the rats to cause ischemia, followed by restoring blood flow. The animals were randomly divided into the control (n=24) and the Gln (n=24) groups for the experiments. The two groups of rats were given enteral nutrition with equal heat, nitrogen (heat 125.4 kJ/kg/day, nitrogen 0.2 g/kg/day). The Gln group of rats was fed with enteral nutrition plus 3% Gln, while the control rats were fed with enteral nutrition plus 3% soybean protein. After 7 days, the HMGB1 and plasma levels of NF-κB, TNF-α, IL-1, Gln, D-lactic acid and diamine oxidase (DAO) were observed. The changes in the morphology of intestinal mucosa were observed using electron microscopy. The plasma levels of TNF-α, IL-1, D-lactic acid and DAO, and the level of HMGB1, NF-κB, TNF-α and IL-1 in intestinal mucosa were significantly higher after IR (p<0.05), while the plasma level of Gln was lower in the two groups. In the control group, the plasma level of IL-1, TNF-α, DAO and D-lactic acid, and that of HMGB1, NF-κB, TNF-α, and IL-1 in intestinal mucosa were significantly higher, while the plasma level of Gln was lower than that prior to modeling on the 3rd and 7th days of the experiment. In the Gln group, the plasma level of IL-1, TNF-α, DAO and D-lactic acid, and that of HMGB1, NF-κB, IL-1, and TNF-α in intestinal mucosa were significantly higher (p<0.05) compared to the control on the 3rd and 7th days of the experiment. By contrast, after the 7th day, the plasma level of IL-1, TNF-α, DAO and D-lactic acid, and the level of HMGB1, NF-κB, IL-1, TNF-α in intestinal mucosa were significantly lower in the Gln group, while the plasma level of Gln was significantly higher than those in control group and after IR on the 7th day of the experiment. Additionally, the structure of villi and recess was damaged, villi was sparse and short, and considerable inflammatory cell influx embellished the lamina propria, lymphangiectasia, and edema after IR. On the 7th day, compared to after IR, the intestinal villi and recess structure of the controls was significantly restored in the Gln group. In conclusion, Gln repaired the intestinal mucosal injury in IR by reducing the expression of HMGB1 and inflammatory cytokines, and...

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Section: Discussionmentioning

confidence: 99%

Glutamine decreases intestinal mucosal injury in a rat model of intestinal ischemia-reperfusion by downregulating HMGB1 and inflammatory cytokine expression

Xiao-liang

Zhang

Wang

et al. 2016

Experimental and Therapeutic Medicine

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“…Multiple pharmacological agents such as iloprost, vitamin C, pentoxifylline and L-alanyl-glutamin are proposed to be useful against renal injury as a remote organ after hindlimb ischemia-reperfusion [2][3][4] .…”

Section: Introductionmentioning

confidence: 99%

Protective effect of N-acetylcysteine on kidney as a remote organ after skeletal muscle ischemia-reperfusion

Takhtfooladi

Jahanshahi

et al. 2012

Acta Cir. Bras.

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PURPOSE: To investigate whether N-acetylcysteine has a protective effect against renal injury as a remote organ after skeletal muscle ischemia-reperfusion in rats. METHODS: Twenty Wistar male rats were divided randomly into two experimental groups: group ischemia-reperfusion (group I) and group ischemia-reperfusion + N-acetylcysteine (group II). After ketamine and xylazine anesthesia, femoral artery was exposed. All animals were undergone 2h of ischemia by occlusion femoral artery and 24h of reperfusion. Rats that were treated with N-acetylcysteine given IV at a dose of 150 mg/kg-¹, immediately before reperfusion. After 24h of reperfusion, the blood samples were collected and submitted for evaluation of plasmatic urea, creatinine values and then rats were euthanized and left kidney harvested for histopathological analysis under light microscopy. RESULTS: The urea (35±7.84 mg.dL-1), creatinine (1.46±0.47 mg.dL-1) values were significantly lower in group II (P=0.000). Renal histopathologic study in group I showed extensive distal and proximal tubular cells necrosis and sloughing of epithelial cells into the tubular lumen, cast formation in tubule and glomerul, glomerul fibrosis and hemorrhage. Histopathologically, there was a significant difference (p=0.037) between two groups. CONCLUSION: The N-acetylcysteine was able to decrease renal injury induced by skeletal muscle ischemia reperfusion in rats.

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“…Published studies showed that administration of L-Gln or L-Ala-Gln in various pathological conditions may enhance both anaerobic [11][12] and aerobic glycolysis 13 . Other researchers have used the infusion of L-Ala-L-Gln associated with parenteral nutrition in Intensive Care Units patients 14 and in patients with traumatic injury 15 .…”

Section: Discussionmentioning

confidence: 99%

Effect of glutamine on the mRNA level of key enzymes of malate-aspartate shuttle in the rat intestine subjected to ischemia reperfusion

Vasconcelos

Neto

Vasconcelos³

et al. 2011

Acta Cir. Bras.

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Effects of L-alanyl-glutamine upon the blood and kidney biochemical parameters in the rat hind limb model of ischemia/reperfusion

Cited by 12 publications

References 11 publications

Glutamine decreases intestinal mucosal injury in a rat model of intestinal ischemia-reperfusion by downregulating HMGB1 and inflammatory cytokine expression

Glutamine decreases intestinal mucosal injury in a rat model of intestinal ischemia-reperfusion by downregulating HMGB1 and inflammatory cytokine expression

Protective effect of N-acetylcysteine on kidney as a remote organ after skeletal muscle ischemia-reperfusion

Effect of glutamine on the mRNA level of key enzymes of malate-aspartate shuttle in the rat intestine subjected to ischemia reperfusion

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