Glutamine treatment attenuates the development of ischaemia/reperfusion injury of the gut

Mondello, Stefania; Galuppo, Maria; Mazzon, Emanuela; Italiano, Domenico; Mondello, Patrizia; Aloisi, Carmela; Cuzzocrea, Salvatore

doi:10.1016/j.ejphar.2010.06.044

Cited by 53 publications

(45 citation statements)

References 42 publications

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“…However, Yuan et al (2011) observed increased levels of serum TNFα 2 hours after reperfusion, although the levels of serum IL-10 decreased in comparison to control. The concentration of pro-inflammatory TNFα on protein level in our study was significantly highest 1 hour after reperfusion, similarly to Mondello et al (2010), whereas after 24 hours and 30 days of reperfusion it showed decreasing tendency probably because of the started regeneration processes. As regards anti-inflammatory IL-10, we observed increased mRNA expression as well as protein concentration 1 hour after reperfusion, probably due to its ability to partially suppress the inevitable inflammatory reaction.…”

Section: A B a Bsupporting

confidence: 50%

Intestinal ischemia-reperfusion injury mediates expression of inflammatory cytokines in rats

Gregová¹,

Číkoš²,

Rabajdová³

et al. 2015

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Abstract. The small intestine is an organ with very well developed immunological activity, responsible for synthesis of specific inflammatory mediators that participate in causing the systemic inflammation that can occur after ischemia-reperfusion injury. The aim of our work was to study mRNA expression and protein concentration of inflammatory cytokines IL-10 and TNFα in the jejunal wall after intestinal ischemia-reperfusion injury (IRI). Cytokine concentration levels confirmed the direct effect of IRI on the inflammation process. The results refer to the changes in balance between pro-inflammatory and anti-inflammatory mediators and indicate that the predominant disturbance of homeostasis after intestinal IRI is present after 1 hour of reperfusion.

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Section: A B a Bsupporting

confidence: 50%

Intestinal ischemia-reperfusion injury mediates expression of inflammatory cytokines in rats

Gregová¹,

Číkoš²,

Rabajdová³

et al. 2015

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“…It has been demonstrated that the attenuation of TNF-α level induces higher expression of antiapoptotic protein Bcl-2 and reduces the expression of cleaved caspase-3, a proapoptotic protein 5,6 . Bearing in mind the results obtained by researchers in the association of HS and PTX in hemorhagic shock and sepsis, we hypothesized that HS and PTX association could protect intestine from mesenteric I/R by increasing antiapoptotic protein and reducing apoptosis deflagration and inflammatory process by reducing cytoplasmic expression of COX-2.…”

Section: Introductionmentioning

confidence: 99%

Pentoxifylline associated to hypertonic saline solution attenuates inflammatory process and apoptosis after intestinal ischemia/reperfusion in rats

Marques

Rasslan²,

Belon³

et al. 2014

Acta Cir. Bras.

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PURPOSE:To evaluate intestinal inflammatory and apoptotic processes after intestinal ischemia/reperfusion injury, modulated by pentoxifylline and hypertonic saline. METHODS:It was allocated into four groups (n=6), 24 male Wistar rats (200 to 250g) and submitted to intestinal ischemia for 40 min and reperfusion for 80 min: IR (did not receive any treatment); HS group (Hypertonic Saline, 4ml/kg-IV); PTX group (Pentoxifylline, 30mg/ kg-IV); HS+PTX group (Hypertonic Saline and Pentoxifylline). All animals were heparinized (100U/kg). At the end of reperfusion, ileal fragments were removed and stained on hematoxylin-eosin and histochemical studies for COX-2, Bcl-2 and cleaved caspase-3. RESULTS:The values of sO 2 were higher on treated groups at 40 minutes of reperfusion (p=0.0081) and 80 minutes of reperfusion (p=0.0072). Serum lactate values were lower on treated groups after 40 minutes of reperfusion (p=0.0003) and 80 minutes of reperfusion (p=0.0098). Morphologic tissue injuries showed higher grades on IR group versus other groups: HS (p=0.0006), PTX (p=0.0433) and HS+PTX (p=0.0040). The histochemical study showed lesser expression of COX-2 (p=0.0015) and Bcl-2 (p=0.0012) on HS+PTX group. A lower expression of cleaved caspase-3 was demonstrated in PTX (p=0.0090; PTXvsIR). CONCLUSION:The combined use of pentoxifylline and hypertonic saline offers best results on inflammatory and apoptotic inhibitory aspects after intestinal ischemia/reperfusion.

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“…21,22 Several reports have demonstrated that prophylactic antiapoptotic treatment is an effective therapeutic strategy for the prevention of intestinal I/R injury. 23,24 In this study, we showed that gastrin could attenuate intestinal crypt cell apoptosis, as evidenced by decline in the apoptotic index, caspase-3 activity and intestinal morphological injury. The antiapoptotic effect of gastrin might be associated with CCK-2 signaling activity.…”

Section: Discussionmentioning

confidence: 97%

Gastrin attenuates ischemia-reperfusion-induced intestinal injury in rats

Liu

Luo

Cheng

et al. 2016

Exp Biol Med (Maywood)

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Intestinal ischemia-reperfusion (I/R) injury is a devastating complication when the blood supply is reflowed in ischemic organs. Gastrin has critical function in regulating acid secretion, proliferation, and differentiation in the gastric mucosa. We aimed to determine whether gastrin has an effect on intestinal I/R damage. Intestinal I/R injury was induced by 60-min occlusion of the superior mesenteric artery followed by 60-min reperfusion, and the rats were induced to be hypergastrinemic by pretreated with omeprazole or directly injected with gastrin. Some hypergastrinemic rats were injected with cholecystokinin-2 (CCK-2) receptor antagonist prior to I/R operation. After the animal surgery, the intestine was collected for histological analysis. Isolated intestinal epithelial cells or crypts were harvested for RNA and protein analysis. CCK-2 receptor expression, intestinal mucosal damage, cell apoptosis, and apoptotic protein caspase-3 activity were measured. We found that high gastrin in serum significantly reduced intestinal hemorrhage, alleviated extensive epithelial disruption, decreased disintegration of lamina propria, downregulated myeloperoxidase activity, tumor necrosis factor-a, and caspase-3 activity, and lead to low mortality in response to I/R injury. On the contrary, CCK-2 receptor antagonist L365260 could markedly impair intestinal protection by gastrin on intestinal I/R. Severe edema of mucosal villi with severe intestinal crypt injury and numerous intestinal villi disintegrated were observed again in the hypergastrinemic rats with L365260. The survival in the hypergastrinemic rats after intestinal I/R injury was shortened by L365260. Finally, gastrin could remarkably upregulated intestinal CCK-2 receptor expression. Our data suggest that gastrin by omeprazole remarkably attenuated I/R induced intestinal injury by enhancing CCK-2 receptor expression and gastrin could be a potential mitigator for intestinal I/R damage in the clinical setting.

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Glutamine treatment attenuates the development of ischaemia/reperfusion injury of the gut

Cited by 53 publications

References 42 publications

Intestinal ischemia-reperfusion injury mediates expression of inflammatory cytokines in rats

Intestinal ischemia-reperfusion injury mediates expression of inflammatory cytokines in rats

Pentoxifylline associated to hypertonic saline solution attenuates inflammatory process and apoptosis after intestinal ischemia/reperfusion in rats

Gastrin attenuates ischemia-reperfusion-induced intestinal injury in rats

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Glutamine treatment attenuates the development of ischaemia/reperfusion injury of the gut

Cited by 53 publications

References 42 publications

Intestinal ischemia-reperfusion injury mediates expression of inflammatory cytokines in rats

Intestinal ischemia-reperfusion injury mediates expression of inflammatory cytokines in rats

Pentoxifylline associated to hypertonic saline solution attenuates inflammatory process and apoptosis after intestinal ischemia/reperfusion in rats

Gastrin attenuates ischemia-reperfusion-induced intestinal injury in rats

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Intestinal ischemia-reperfusion injury mediates expression of inflammatory cytokines in rats

Intestinal ischemia-reperfusion injury mediates expression of inflammatory cytokines in rats