Intestinal ischemia/reperfusion causes tissue hypoxia and damage, leading to the pathophysiology of inflammation. The aim of this study was to investigate the effects of glutamine on the tissue injury caused by ischemia/reperfusion of the gut. Ischemia/reperfusion injury of the intestine was caused by clamping both the superior mesenteric artery and the celiac trunk for 30 min followed by the release of the clamp allowing reperfusion for 1h. This procedure results in splanchnic artery occlusion-injury. Based on our findings we propose that the amino acid glutamine, administered 15 min before reperfusion at the dose of 1.5mg/kg, i.v. may be useful in the treatment of various ischemia and reperfusion diseases. The present study was performed in order to determine the pharmacological effects of glutamine ischemia/reperfusion-induced intestinal injury in rats. In particular, to gain a better insight into the mechanism(s) of action of glutamine, we evaluated the following endpoints of the inflammatory response: (1) histological damage; (2) neutrophil infiltration of the reperfused intestine (MPO activity); (3) NF-kappaB activation and cytokines production; (4) expression of ICAM-1 and P-selectin during reperfusion; (5) nitrotyrosine and poly-ADP-ribose formation; (6) pro-inflammatory cytokine production; (7) inducible nitric oxide synthase expression; (8) apoptosis as shown by TUNEL staining and (9) Bax/Bcl-2 expression.
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http://dx.doi.org/10.1016/j.ejphar.2010.06.044 | DOI Listing |
Neurotox Res
January 2025
Programa de Pós-Graduação em Ciências Biológicas: Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
Resveratrol, a natural polyphenol, has shown promising neuroprotective effects in several in vivo and in vitro experimental models. However, the mechanisms by which resveratrol mediates these effects are not fully understood. Glutamate is the major excitatory neurotransmitter in the brain; however, excessive extracellular glutamate levels can affect neural activity in several neurological diseases.
View Article and Find Full Text PDFBackground: Targeting glutamine metabolism has emerged as a promising strategy in cancer therapy. However, several barriers, such as anti-tumor efficacy, drug toxicity, and safety, remain to be overcome to achieve clinical utility. Prior preclinical studies had generated encouraging data showing promises of cancer metabolism targeting drugs, although most were performed on immune-deficient murine models.
View Article and Find Full Text PDFJ Agric Food Chem
January 2025
Institute of Quality Standard and Testing Technology for Agro-Products, Shandong Academy of Agricultural Sciences, Jinan 250100, Shandong, China.
γ-l-Glutamyl-S-allyl-l-cysteine (GSAC) is renowned for its flavor-modifying effects and beneficial biological activities. However, the level of GSAC decreases significantly during the processing of black garlic, and the pathways and degradation products resulting from this decline remain unclear. To investigate the potential transformation mechanisms of GSAC in black garlic, simulation systems for thermal decomposition, Maillard reactions, and enzymatic hydrolysis were established.
View Article and Find Full Text PDFBiosci Trends
January 2025
School of Pharmacy, Sungkyunkwan University, Suwon, Korea.
Alzheimer's disease (AD) is the most common type of dementia. Its incidence is rising rapidly as the global population ages, leading to a significant social and economic burden. AD involves complex pathologies, including amyloid plaque accumulation, synaptic dysfunction, and neuroinflammation.
View Article and Find Full Text PDFFoods
January 2025
Department of Food Bioengineering, Jeju National University, Jeju 63243, Republic of Korea.
In this study, we explored the binding mechanism between tannic acid (TA) and gluten to apply TA as an ingredient in bread-making to evaluate its baking performance and starch digestion. The interaction was systematically investigated by analyzing binding affinity, binding mode, and matrix structure of the TA-gluten complex using fluorescence quenching, molecular docking, and confocal laser scanning microscopy. TA strongly interacted with gluten via non-covalent interactions, mainly hydrogen bonds, and formed the major hydrogen bonds with six different glutamines (Q32, Q108, Q313, Q317, Q317, and Q349), which play a critical role in gluten network construction among amino acid residues of gluten.
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