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glutamine/infiammazione
Il collegamento viene salvato negli appunti
Pagina 1 a partire dal 1418 risultati
Glutamine protects against LPS-induced inflammation via adjusted NODs signaling and enhanced immunoglobulins secretion in rainbow trout leukocytes.
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To evaluate effects of glutamine (GLN) on fish immune responses, leukocytes were isolated from head kidney of rainbow trout and cultured in GLN-free DMEM media supplemented with different combinations of lipopolysaccharide (LPS) and GLN. LPS significantly increased expression of pro-inflammatory
Use of butyrate or glutamine in enema solution reduces inflammation and fibrosis in experimental diversion colitis.
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OBJECTIVE
To investigate whether butyrate or glutamine enemas could diminish inflammation in experimental diversion colitis.
METHODS
Wistar specific pathogen-free rats were submitted to a Hartmann's end colostomy and treated with enemas containing glutamine, butyrate, or saline. Enemas were
Alanyl-glutamine improves pancreatic β-cell function following ex vivo inflammatory challenge.
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Obesity-associated diabetes and concomitant inflammation may compromise pancreatic β-cell integrity and function. l-glutamine and l-alanine are potent insulin secretagogues, with antioxidant and cytoprotective properties. Herein, we studied whether the dipeptide l-alanyl-l-glutamine (Ala-Gln) could
Pigment epithelium derived factor as an anti-inflammatory factor against decrease of glutamine synthetase expression in retinal Müller cells under high glucose conditions.
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BACKGROUND
The pathogenesis of diabetic retinopathy (DR) is similar to that of a chronic inflammatory disease. A predominant function of Müller cells is to regulate glutamate levels, but in DR the function is compromised. The present study was performed to investigate the role of pigment epithelial
Glutamine preferentially inhibits T-helper type 2 cell-mediated airway inflammation and late airway hyperresponsiveness through the inhibition of cytosolic phospholipase A(2) activity in a murine asthma model.
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BACKGROUND
The non-essential amino acid, l-glutamine (Gln), is abundant in the human body. Gln exhibits beneficial effects on endotoxic shock through the inhibition of cytosolic phospholipase A(2) (cPLA(2)) activity. cPLA(2) has been reported to be implicated in the pathogenesis of asthma, but the
Glutamine Administration After Sublethal Lower Limb Ischemia Reduces Inflammatory Reaction and Offers Organ Protection in Ischemia/Reperfusion Injury.
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This study investigated the effects of intravenous glutamine (GLN) administration on the expression of adhesion molecules and inflammatory mediators in a mice model of hind limb ischemia/reperfusion (IR) injury.
There were 3 IR groups and 1 normal control (NC) group. The NC group did not undergo the
Short communication: Glutamine modulates inflammatory responses to lipopolysaccharide in ex vivo bovine endometrium.
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Bacteria infect the endometrium lining the uterus of cattle after parturition, and clearance of these microbes depends on a robust innate immune response to bacterial molecules, such as the endotoxin lipopolysaccharide (LPS). Endometrial inflammation is characterized by secretion of the cytokines
Enzymes of glutamine metabolism in inflammation associated with skeletal muscle hypertrophy.
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Glutamine synthesis and utilization were studied in the plantaris muscle after removal of its functional synergists, the soleus and gastrocnemius muscles. Rat plantaris muscle was compared with unoperated controls at 7, 14, and 30 days after synergist ablation and induction of hypertrophy. Glutamine
Hepatic uptake of glutamine and other amino acids during infection and inflammation.
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Catabolic illness such as sepsis and injury induce profound changes in host amino acid metabolism, including increased hepatic amino acid uptake. Because many amino acid-dependent pathways such as gluconeogenesis and acute-phase protein synthesis are activated in the liver during severe infection,
[Comparative study of the evolution of inflammatory colitis treated with an elemental diet, glutamine and 5-ASA. An experimental study in rats].
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The objective of the present investigation was to study the evolution of untreated inflammatory disease of the colon as compared to disease treated with an elemental diet plus glutamine, with 5-ASA and with a combination of the three. A total of 120 female Wistar-Tecpar rats aged 180 days and
Impact of alanyl-glutamine dipeptide on proliferative and inflammatory changes in jejunal mucosa after acute mesenteric ischemia.
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OBJECTIVE
The aim of our study was to determinate the impact of dipeptide (alanyl-glutamine) administration on inflammatory and proliferative changes in jejunal mucosa after acute mesenteric ischemia.
METHODS
Male Wistar rats (n=30) were divided into three groups: ischemia/reperfusion (IR) group
Alanyl-glutamine administration suppresses Th17 and reduces inflammatory reaction in dextran sulfate sodium-induced acute colitis.
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T helper (Th) cells play a major role in the pathogenesis of inflammatory bowel disease (IBD). Glutamine (Gln) is known to have immunomodulatory effects in metabolic stressed conditions. This study investigated the effects of post-treatment of alanyl-glutamine (Ala-Gln) on Th cell-associated
Glutamine decreases lipopolysaccharide-induced intestinal inflammation in infant rats.
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Using a gastrostomy-fed (GF) rat infant "pup-in-a-cup" model, the effects of protein deprivation and supplemental glutamine (Gln) and glutamate (Glu) were examined to test the hypothesis that Gln decreases the proinflammatory response induced by LPS in the developing infant rat small intestine. Four
Effect of N-acetyl-L-glutamine aluminum complex (KW-110), an antiulcer agent, on the non-steroidal anti-inflammatory drug-induced exacerbation of gastric ulcer in rats.
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Gastric ulcer induced by the injection of acetic acid (0.025 ml of 20%) into the gastric wall of rats was healed considerably 5 days after the injection of acetic acid. Non-steroidal anti-inflammatory drugs (NSAID) such as aspirin, indomethacin, and phenylbutazone were given consecutively for 5
Inflammatory cytokine TNF-α inhibits Na(+)-glutamine cotransport in intestinal epithelial cells.
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Glutamine (Gln), a preferred fuel source for enterocytes, is critical for intestinal epithelial cell integrity and barrier function. Chronic enteritis inhibits apical Na(+)-Gln cotransport. It is not known whether inflammatory cytokines that are secreted during inflammation inhibit Na(+)-Gln
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