Effects of glutamine alone on the acute necrotizing pancreatitis in rats

Alhan, Etem; Usta, Arif; Türkyılmaz, Serdar; Kural, Birgül Vanizör; Erçín, Cengiz

doi:10.1016/j.jss.2014.07.029

Cited by 7 publications

(5 citation statements)

References 46 publications

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“…1,2,4,8,15 The role of oxidative stress in the pathogenesis of AP and the benefits of antioxidants have been the subject of numerous studies. 14,[16][17][18][19] Recent studies have focused on antioxidant and anti-inflammatory properties of phenolic compounds. 2,4,6,20 Quercetin (3,5,7,3',4' pentahydroxyflavone) is a plant-derived phenolic compound belonging to a class of substances known as flavonoids.…”

Section: Methodsmentioning

confidence: 99%

The effect of quercetin on cerulein-induced acute pancreatitis

Kahraman¹,

Vurmaz²,

Koca³

et al. 2017

Medical Express

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OBJECTIVE:The aim of this study was to evaluate the protective and therapeutic effects of quercetin on pancreatic injury in cerulein-induced acute pancreatitis. METHOD: Thirty-two rats were randomly divided into four groups, eight per group: (CT): untreated controls, (CER) treated with cerulein, 50 μg/kg body weight; (Q+CER) pre-treatment with quercetin, 100 mg/kg body weight, followed by cerulein, 50 μg/kg; (CER+Q) post-treatment, cerulein followed by quercetin, same doses. Cerulein was divided into four doses, given at 1-hour intervals by intraperitoneal injection. Quercetin was given either 1-hour before (in pre-treatment group) or 1-hour after (in post-treatment group) cerulein. Pancreatic malondialdehyde (MDA), carbonyl, myeloperoxidase (MPO), tumor necrosis factor-alpha (TNF-a), interleukin-6 (IL-6), reduced and oxidized glutathione (GSH and GSSG, respectively) were measured. Histology of the pancreas was studied. RESULTS: (1) MDA, carbonyl, MPO, TNF-a and IL-6 levels were significantly higher in CER vs CT rats. (2) MDA, carbonyl, MPO and TNF-α decreased significantly in pre-treated rats vs. CER. (3) MDA, MPO, TNF-α, IL-6 were significantly lower in post-treated rats vs. CER. (4) The reduced vs. oxidized glutathione ratio (GSH/GSSG) of was significantly lower CER vs. CT rats. (5) Pre-and post-treatment with quercetin significantly increased this ratio. (6) Pancreatic histology showed that quercetin had no significant effect on the histological image of the pancreas CONCLUSION: These results suggest that quercetin can attenuate the severity of cerulein-induced acute pancreatitis by acting as an antioxidant and anti-inflammatory agent and combating oxidative stress. Further studies are needed to clearly explain its utility on acute pancreatitis.

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Section: Methodsmentioning

confidence: 99%

The effect of quercetin on cerulein-induced acute pancreatitis

Kahraman¹,

Vurmaz²,

Koca³

et al. 2017

Medical Express

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“…It has a powerful glycemic effect which can provide sufficient substrates for oxidative phosphorylation of the cells. Gln can be administered to maintain gut integrity and ameliorate the inflammatory response in AP [17–19]. Our results indicated that Gln supplementation in addition to HIF-1 α knockdown was more protective for the acinar cells from AP-related injuries than HIF-1 α knockdown alone was.…”

Section: Discussionmentioning

confidence: 76%

“…Gln is a source of fuel for lymphocytes and enterocytes and might play an antioxidative role as a precursor for glutathione and a cytoprotective role by upregulating heat shock proteins [16]. It has been shown that Gln supplementation during AP maintains gut integrity, improves the immune response, and decreases the release of some proinflammatory mediators by inhibiting the activation of nuclear factor-kappa B (NF- κ B) and p38 mitogen-activated protein kinase [17–19]. On the basis of the solubility and instability of Gln, L-alanyl-L-glutamine is usually administered as a donor in vivo because it is a dipeptide that dissociates into free Gln soon after entry into the circulatory system [20].…”

Section: Introductionmentioning

confidence: 99%

Hypoxia-Inducible Factor-1αKnockdown Plus Glutamine Supplementation Attenuates the Predominance of Necrosis over Apoptosis by Relieving Cellular Energy Stress in Acute Pancreatitis

Guo

et al. 2019

Oxidative Medicine and Cellular Longevity

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The present study was conducted to investigate the effect and potential mechanism of hypoxia-inducible factor-1α (HIF-1α) genetic inhibition plus glutamine (Gln) supplementation on necrosis-apoptosis imbalance during acute pancreatitis (AP), with a specific focus on the regulations of intracellular energy metabolism status. Wistar rats and AR42J cells were used to establish AP models. When indicated, a HIF-1α knockdown with or without a Gln supplementation was administered. In vivo, local and systemic inflammatory injuries were assessed by serum cytokine measurement, H&E staining, and transmission electron microscope (TEM) observation of pancreatic tissue. In vitro, intracellular energy metabolism status was evaluated by measuring the intracellular adenosine triphosphate (ATP), lactic acid, and Ca2+ concentrations and the mitochondrial potential. In addition, changes in the apoptotic activity were analyzed using TUNEL staining in vivo and an apoptosis assay in vitro. HIF-1α knockdown alleviated AP-related inflammatory injury as indicated by the measurements of serum cytokines and examinations of TEM and H&E staining of pancreatic tissues. HIF-1α knockdown played an antioxidative role against AP-related injuries by preventing the increase in the intracellular Ca2+ concentration and the decrease in the mitochondrial membrane potential and subsequently by suppressing the glycolysis pathway and increasing energy anabolism in AR42J cells after AP induction. Apoptosis was significantly upregulated when HIF-1α was knocked down before AP induction due to an attenuation of the translocation of nuclear factor-kappa B to the nuclei. Furthermore, these merits of HIF-1α knockdown in the relief of the metabolic stress and upregulation of apoptosis were more significant when Gln was administered concomitantly. In conclusion, Gln-supplemented HIF-1α knockdown might be promising for the future management of AP by relieving the intracellular energy stress, thereby attenuating the predominance of necrosis over apoptosis.

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“…The analytical approaches, pathological features, and common measurements have been described in a recent review (3). In severe models of AP, liver/kidney malfunction can also be monitored and has been described (6,12).…”

Section: Animal Models Of Acute Pancreatitismentioning

confidence: 99%

Animal models of gastrointestinal and liver diseases. Animal models of acute and chronic pancreatitis

Zhan

Wang

et al. 2016

American Journal of Physiology-Gastrointestinal and Liver Physi

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Animal models of pancreatitis are useful for elucidating the pathogenesis of pancreatitis and developing and testing novel interventions. In this review, we aim to summarize the most commonly used animal models, overview their pathophysiology, and discuss their strengths and limitations. We will also briefly describe common animal study procedures and refer readers to more detailed protocols in the literature. Although animal models include pigs, dogs, opossums, and other animals, we will mainly focus on rodent models because of their popularity. Autoimmune pancreatitis and genetically engineered animal models will be reviewed elsewhere.

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Effects of glutamine alone on the acute necrotizing pancreatitis in rats

Cited by 7 publications

References 46 publications

The effect of quercetin on cerulein-induced acute pancreatitis

The effect of quercetin on cerulein-induced acute pancreatitis

Hypoxia-Inducible Factor-1αKnockdown Plus Glutamine Supplementation Attenuates the Predominance of Necrosis over Apoptosis by Relieving Cellular Energy Stress in Acute Pancreatitis

Animal models of gastrointestinal and liver diseases. Animal models of acute and chronic pancreatitis

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