Glutamine Reduces Cytokine Release, Organ Damage, and Mortality in a Rat Model of Endotoxemia

Wischmeyer, Paul E.; Kahana, Madelyn; Wolfson, Rachel L.; Ren, Hao; Musch, M.; Chang, Eugene B.

doi:10.1097/00024382-200116050-00014

Cited by 155 publications

(116 citation statements)

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“…Glutamine has been demonstrated to protect cells and tissues from diverse forms of cellular stress and tissue injury (Wischmeyer et al 2001). As glutamine is utilized by the HBP in the generation of UDP-GlcNAc (Fig.…”

Section: Heat Shock Protein Expressionmentioning

confidence: 99%

Dynamic O-GlcNAcylation and its roles in the cellular stress response and homeostasis

Groves

Lee

Yildirir

et al. 2013

Cell Stress and Chaperones

114

105

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O-linked N-acetyl-β-D-glucosamine (O-GlcNAc) is a ubiquitous and dynamic post-translational modification known to modify over 3,000 nuclear, cytoplasmic, and mitochondrial eukaryotic proteins. Addition of O-GlcNAc to proteins is catalyzed by the O-GlcNAc transferase and is removed by a neutral-N-acetyl-β-glucosaminidase (OGlcNAcase). O-GlcNAc is thought to regulate proteins in a manner analogous to protein phosphorylation, and the cycling of this carbohydrate modification regulates many cellular functions such as the cellular stress response. Diverse forms of cellular stress and tissue injury result in enhanced O-GlcNAc modification, or O-GlcNAcylation, of numerous intracellular proteins. Stress-induced OGlcNAcylation appears to promote cell/tissue survival by regulating a multitude of biological processes including: the phosphoinositide 3-kinase/Akt pathway, heat shock protein expression, calcium homeostasis, levels of reactive oxygen species, ER stress, protein stability, mitochondrial dynamics, and inflammation. Here, we will discuss the regulation of these processes by O-GlcNAc and the impact of such regulation on survival in models of ischemia reperfusion injury and trauma hemorrhage. We will also discuss the misregulation of O-GlcNAc in diseases commonly associated with the stress response, namely Alzheimer's and Parkinson's diseases. Finally, we will highlight recent advancements in the tools and technologies used to study the O-GlcNAc modification.

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Section: Heat Shock Protein Expressionmentioning

confidence: 99%

Dynamic O-GlcNAcylation and its roles in the cellular stress response and homeostasis

Groves

Lee

Yildirir

et al. 2013

Cell Stress and Chaperones

114

105

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“…It was reported that rhoifolin has protective effects on the renal cellular membrane and able to ameliorate renal cellular injury. It also exerts anti-diabetic effect through enhanced adiponectin secretion, phosphorylation of insulin receptor-β, and GLUT4 translocation (Yokozawa et al, 1999). Furthermore, its hepatoprotective effect was reported against carbon tetrachloride induce hepatotoxicity in mice (Perez Gutierrez et al, 2011).…”

Section: Introductionmentioning

confidence: 97%

Anti-inflammatory Effect of Apigenin-7-neohesperidoside (Rhoifolin) in Carrageenin-Induced Rat Oedema Model

Eldahshan¹

2012

J. App. Pharm. Sci.

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Flavonoids are normal constituents of the human diet and are known for a variety of biological activities. They have been reported to bring benefits in lowering inflammation and oxidative stress. The present investigation was performed first, to evaluate the anti-inflammatory activity of rhoifolin and second, to search for the possible contributing mechanisms for this hypothesized effect. Rhoifolin caused a time and reverse dose dependent reduction of carrageenin-induced rat paw oedema. Following 4 hr of treatment, rhoifolin at doses 2.5, 25 & 250 mg/kg caused a significant inhibition of rat paw edema volume by 14, 25 & 45 % respectively in comparison to the control group (74%). In addition to significantly abrogating prostaglandin E2 level, increasing doses of rhoifolin significantly diminished the TNF-α release in the inflammatory exudates. In the same animal model, rhoifolin increased the total antioxidant capacity in a reverse dose order, with the highest capacity obtained with the lowest dose tested. This study demonstrates for the first time the effectiveness of rhoifolin in combating inflammation in carrageenin-induced rat oedema model.

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“…Gln was dissolved in sterilized distilled water to 3%. A volume of 0Á5 ml (750 mg/ kg) [12][13][14][15] was administered intraperitoneally (i.p.) 10 min before or 10 min after LPS injection.…”

Section: Reagentsmentioning

confidence: 99%

Mechanism of glutamine inhibition of cytosolic phospholipase a2 (cPLA2): Evidence of physical interaction between glutamine-Induced mitogen-activated protein kinase phosphatase-1 and cPLA2

Lee

Kim

Jeong

et al. 2015

Clinical and Experimental Immunology

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SummaryNon-essential amino acid L-glutamine (Gln) possesses anti-inflammatory activity via deactivating cytosolic phospholipase A 2 (cPLA 2 ). We showed previously that Gln deactivated cPLA 2 indirectly via dephosphorylating p38 mitogen-activated protein kinase (MAPK), the major kinase for cPLA 2 phosphorylation, through inducing MAPK phosphatase-1 (MKP-1). In this study, we investigated the precise mechanism underlying Gln deactivation of cPLA 2 . In lipopolysaccharide (LPS)-treated mice, Gln injection resulted in dephosphorylation of phosphorylated cPLA 2 (p-cPLA 2 ), which coincided with rapid Gln induction of MKP-1. MKP-1 small interfering RNA (siRNA) abrogated the ability of Gln to induce MKP-1 as well as the dephosphorylation of cPLA 2 . Co-immunoprecipitation and in-situ proximity ligation assay revealed a physical interaction between MKP-1 and p-cPLA 2 . In a murine model of allergic asthma, we also demonstrated the physical interaction between MKP-1 and p-cPLA 2 . Furthermore, Gln suppressed various allergic asthma phenotypes, such as neutrophil and eosinophil recruitments into the airway, airway levels of T helper type 2 (Th2) cytokines [interleukin (IL)-4, IL-5 and IL-13], airway hyperresponsiveness, mucin production and metabolites (leukotriene B 4 and platelet-activating factor) through inhibiting cPLA 2 in a MKP-1-dependent manner. These data suggest that MKP-1 uses cPLA 2 , in addition to p38, as a substrate, which further potentiates the anti-inflammatory action of Gln.

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Glutamine Reduces Cytokine Release, Organ Damage, and Mortality in a Rat Model of Endotoxemia

Cited by 155 publications

References 0 publications

Dynamic O-GlcNAcylation and its roles in the cellular stress response and homeostasis

Dynamic O-GlcNAcylation and its roles in the cellular stress response and homeostasis

Anti-inflammatory Effect of Apigenin-7-neohesperidoside (Rhoifolin) in Carrageenin-Induced Rat Oedema Model

Mechanism of glutamine inhibition of cytosolic phospholipase a2 (cPLA2): Evidence of physical interaction between glutamine-Induced mitogen-activated protein kinase phosphatase-1 and cPLA2

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