beta glucuronidase/inflammation

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In vivo evaluation of [18F]FEAnGA-Me: a PET tracer for imaging β-glucuronidase (β-GUS) activity in a tumor/inflammation rodent model.

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BACKGROUND The PET tracer, 1-O-(4-(2-fluoroethyl-carbamoyloxymethyl)-2-nitrophenyl)-O-β-d-glucopyronuronate ([(18)F]FEAnGA), was recently developed for PET imaging of extracellular β-glucuronidase (β-GUS). However, [(18)F]FEAnGA exhibited rapid renal clearance, which resulted in a relatively low

Beta-glucuronidase and Beta-glucosidase activity in stool specimens of children with inflammatory bowel disease.

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The aim of the study was to analyze the differences in the activity of beta-glucuronidase and beta-glucosidase in stool specimens of children with Inflammatory Bowel Diseases (IBD) and healthy subjects. The disease activity was determined according to the PCDAI scale (Crohn disease) and

β-Glucuronidase, a Regulator of Lyme Arthritis Severity, Modulates Lysosomal Trafficking and MMP-9 Secretion in Response to Inflammatory Stimuli.

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The lysosomal enzyme β-glucuronidase (Gusb) is a key regulator of Lyme-associated and K/B×N-induced arthritis severity. The luminal enzymes present in lysosomes provide essential catabolic functions for the homeostatic degradation of a variety of macromolecules. In addition to this essential

Kinetic study of neutrophil and inflammatory fluid beta glucuronidase.

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Beta glucuronidase obtained from rat inflammatory fluid and granulocytes was studied kinetically. Linear increases in activity occurred with time and enzyme concentration. No evidence of enzyme degradation during incubation was obtained. Supernatant and granulocyte enzyme activity was identical in

[Importance of beta-glucuronidase activity and glycosaminoglycan concentration in synovial fluid in patients with rheumatoid arthritis in estimating local inflammation].

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In 30 patients with rheumatoid arthritis, the activity of beta-glucuronidase and the content of sulfated and non-sulfated glycosaminoglycans (GAG) were measured in synovial fluid (SF) and in the cells of SF. It has been established that as the local inflammation increases, the activity of the enzyme

Inflammation-associated extracellular β-glucuronidase alters cellular responses to the chemical carcinogen benzo[a]pyrene.

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Neutrophils infiltrate tissues during inflammation, and when activated, they release β-glucuronidase. Since inflammation is associated with carcinogenesis, we investigated how extracellular β-glucuronidase changed the in vitro cellular response to the chemical carcinogen benzo(a)pyrene (B[a]P). For

Bacterial β-glucuronidase alleviates dextran sulfate sodium-induced colitis in mice: A possible crucial new diagnostic and therapeutic target for inflammatory bowel disease.

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Inflammatory bowel diseases (IBD) including ulcerative colitis and Crohn's disease are devastating diseases of the gut. At present, all the treatments are mainly targeting symptoms like inflammation. The disease remains regarded as incurable, largely due to lacking of knowledge on its

In vivo evaluation of 1-O-(4-(2-fluoroethyl-carbamoyloxymethyl)-2-nitrophenyl)-O-β-D-glucopyronuronate: a positron emission tomographic tracer for imaging β-glucuronidase activity in a tumor/inflammation rodent model.

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β-Glucuronidase (β-GUS) plays an important role in inflammation and degenerative processes. The enzyme has also been investigated as a target in prodrug therapy for cancer. To investigate the role of β-GUS in pathologies and to optimize β-GUS-based prodrug therapies, we recently developed a positron

Pharmacologic targeting of bacterial β-glucuronidase alleviates nonsteroidal anti-inflammatory drug-induced enteropathy in mice.

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Small intestinal mucosal injury is a frequent adverse effect caused by nonsteroidal anti-inflammatory drugs (NSAIDs). The underlying mechanisms are not completely understood, but topical (luminal) effects have been implicated. Many carboxylic acid-containing NSAIDs, including diclofenac (DCF), are

β-Glucuronidase activity and mitochondrial dysfunction: the sites where flavonoid glucuronides act as anti-inflammatory agents.

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Epidemiological and experimental studies suggest that the consumption of flavonoid-rich diets decreases the risk of various chronic diseases such as cardiovascular diseases. Although studies on the bioavailability of flavonoids have been well-characterized, the tissue and cellular localizations

[Inflammatory reaction to polyester material in the guinea pig. IV. Production and liberation of beta glucuronidase and lactate dehydrogenase by peritoneal macrophages in culture].

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Peritoneal macrophages obtained from guinea pigs intraperitoneally injected with minced polyester threads with saline, and from control animals were cultivated and the activities of the lysosomal enzyme beta-glucuronidase and of the cytoplasmic enzyme lactate dehydrogenase were determined in the

Antineutrophil Cytoplasmic Antibodies in Inflammatory Bowel Disease and Collagenous Colitis: No Association with Lactoferrin, β-Glucuronidase, Myeloperoxidase, or Proteinase 3.

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: Perinuclear antineutrophil cytoplasmic antibodies (P-ANCA) occur frequently in ulcerative colitis (UC) but not in Crohn's disease (CD). Their pathogenetic importance is unknown, and studies of associated antigens have been inconsistent. Indirect immunofluorescence technique was used to screen the

Perinuclear Antineutrophil Cytoplasmic Antibody with a Large Portion Being Anti-β-Glucuronidase, May Have Played a Causative Role in the Pathogenesis of Inflammatory Bowel Disease.

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Histochemical demonstration of beta-glucuronidase activity in experimental inflammation produced by croton oil in rats.

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Effects of anti-inflammatory and immuno-modulating agents on the release of beta-glucuronidase and collagenase from cultured macrophages of guinea pigs.

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