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hexosamine/възпаление
Линкът е запазен в клипборда
Страница 1 от 144 резултата
Hexosamine biosynthesis pathway flux promotes endoplasmic reticulum stress, lipid accumulation, and inflammatory gene expression in hepatic cells.
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There is increasing evidence that endoplasmic reticulum (ER) stress contributes to the development of atherosclerosis in diabetes mellitus. The purpose of this study was to determine the effects of increased hexosamine biosynthesis pathway (HBP) flux on ER stress levels and the complications of ER
The hexosamine biosynthesis inhibitor azaserine prevents endothelial inflammation and dysfunction under hyperglycemic condition through antioxidant effects.
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Hexosamine biosynthetic pathway (HBP) accounts for some cardiovascular adverse effects of hyperglycemia. We investigated whether the HBP inhibitor azaserine protects against hyperglycemia-induced endothelial damage dependently of HBP. Human endothelial cells isolated from umbilical veins were
Glycolysis and the Hexosamine Biosynthetic Pathway as Novel Targets for Upper and Lower Airway Inflammation.
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Glycolysis is a process that rapidly converts glucose to lactate to produce adenosine triphosphate (ATP) under anaerobic conditions and occurs in all eukaryotic and prokaryotic cells. On the other hand, the hexosamine biosynthetic pathway (HBP) converts glucose to intermediate products like
[Biochemistry of inflammation. I. The hexosamines at the level of Arthus and Shwartzman skin reactions].
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[The effect of various anti-inflammatory agents on serum hexosamine level in experimental radiation pneumonia].
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Effect of two non-steroidal anti-inflammatory agents on hexosamine and sialic acid contents of inflamed tissue.
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[Changes in glycosaminoglycans and glycoproteins during development of proliferative inflamed tissue and effect of anti-inflammatory drugs on the metabolism of these hexosamine-containing substances (author's transl)].
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Proceedings: The actions of some anti-inflammatory and antirheumatic drugs on hexosamine biosynthesis.
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Inhibitory effect on bone formation and calcification exerted by the anti-inflammatory drug ibuprofen. An experimental study on adult rat with fracture.
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The anti-inflammatory drug ibuprofen (2-(4-isobutylfenyl)propionic acid) was administered to adult male rats for 10 weeks in daily oral doses of 16 mg. Fractured and unfractured tibias were studied during 4 to 10 weeks' treatment by the use of microradiography, fluorescence labelling and
Urinary excretion of connective tissue metabolites under the influence of a new non-steroidal anti-inflammatory agent in adjuvant induced arthritis.
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The therapeutic effect of boswellic acids and salai guggal in adjuvant induced arthritic rats in relation to urinary excretion of connective tissue metabolites viz. hydroxyproline, hexosamine and uronic acid was thoroughly investigated. Compared to controls, the arthritic animals showed an increase
O-linked beta-N-acetylglucosamine during hyperglycemia exerts both anti-inflammatory and pro-oxidative properties in the endothelial system.
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Elevated cellular levels of protein O-linked beta-N-acetylglucosamine (O-GlcNAc) through hexosamine biosynthesis pathway (HBP) are suggested to contribute to cardiovascular adverse effects under chronic hyperglycemic condition associated with oxidative stress and inflammation. Conversely, enhancing
Favourable modulation of the inflammatory changes in hypercholesterolemic atherogenesis by a low-molecular-weight heparin derivative.
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BACKGROUND
In the hypercholesterolemic state, the net result of combined oxidative and nitrosative stress is a pro-inflammatory phenotype that is manifested as increased adhesion molecule expression, enhanced leucocyte trafficking, and increased vascular permeability. The present work explores the
The hexosamine biosynthesis pathway negatively regulates IL-2 production by Jurkat T cells.
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To test the hypothesis that the hexosamine biosynthesis pathway (HBP) affects cytokine production, we studied IL-2 production by Jurkat cells in response to PHA. We found that the HBP activator glucosamine (GlcN), but not glucose (Glc), dose-dependently reduced IL-2 production. Importantly, GlcN
Studies on the metabolism of glycosaminoglycans under the influence of new herbal anti-inflammatory agents.
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The in vivo effect of an herbal based, non-steroidal anti-inflammatory product, salai guggal, prepared from the gum resin exudate of Boswellia serrata and its active principle "boswellic acids" on glycosaminoglycan metabolism has been studied in male albino rats. The biosynthesis of sulfated
Exacerbation of acetic acid ulcer induced by non-steroidal anti-inflammatory drugs in rats.
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The influences of non-steroidal anti-inflammatory drugs (NSAID) on acetic acid ulcer were examined in rats. NSAID used in this study were aspirin (ASP, 200 mg/kg), indomethacin (IND, 2 mg/kg) and phenylbutazone (PHE, 100 mg/kg). These NSAID were administered consecutively for 5 days once a day at
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