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Xanthine Oxidase Inhibitors (xanthine + oxidase_inhibitor)

Distribution by Scientific Domains

Medical Sciences	60%

Selected Abstracts

Role of xanthine oxidase in small bowel mucosal dysfunction after surgical stress

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 8 2000
R. Anup
Background The small intestine is highly susceptible to surgical stress even at remote locations. An earlier study using a rat model indicated that oxidative stress plays an important role in this process. The enzyme xanthine oxidase is an important source of free radicals in the small intestine. The role of this enzyme in intestinal damage after surgical stress was examined. Methods Rats pretreated with xanthine oxidase inhibitors were subjected to surgical stress by opening the abdomen and handling the intestine, as done during laparotomy. Enterocytes at various stages of differentiation were isolated and the protection offered by xanthine oxidase inhibitors against damage due to surgical stress was determined and compared with normal controls. Protection against ultrastructural changes to the mucosa, as well as mitochondrial function was examined. Results Surgical stress affected both the villus as well as crypt cells, causing increased superoxide generation, accompanied by increased activity of xanthine oxidase. Xanthine oxidase inhibitors ameliorated the increased superoxide generation, and protected against mitochondrial damage and ultrastructural changes in the intestine. Conclusion Surgical stress affects both the villus and crypt cell populations in the small intestine. The enzyme xanthine oxidase maybe an important mediator of surgical stress in the intestine. © 2000 British Journal of Surgery Society Ltd [source]

Conversion of Th17-type into Th2-type inflammation by acetyl salicylic acid via the adenosine and uric acid pathway in the lung

ALLERGY, Issue 9 2010
H.-G. Moon
To cite this article: Moon H-G, Tae Y-M, Kim Y-S, Gyu Jeon S, Oh S-Y, Song Gho Y, Zhu Z, Kim Y-K. Conversion of Th17-type into Th2-type inflammation by acetyl salicylic acid via the adenosine and uric acid pathway in the lung. Allergy 2010; 65: 1093,1103. Abstract Background:, Allergen-specific T-cell responses orchestrate airway inflammation, which is a characteristic of asthma. Recent evidence suggests that noneosinophilic asthma can be developed by mixed Th1 and Th17 cell responses when exposed to lipopolysaccharide (LPS)-containing allergens. Objective:, To evaluate the therapeutic or adverse effects of acetyl salicylic acid (ASA) on the expression of Th1-type and Th17-type inflammation induced by airway exposure to LPS-containing allergens. Methods:, Th1 + Th17 asthma and Th2 asthma mouse models were generated by intranasal sensitization with ovalbumin (OVA) and LPS and intraperitoneal sensitization with OVA and alum, respectively. Therapeutic or adverse effects were evaluated after allergen challenge using pharmacologic and transgenic approaches. Results:, Lung infiltration of eosinophils was enhanced in OVA/LPS-sensitized mice by ASA treatment, which was accompanied by the enhanced production of eotaxin. These changes were associated with the down-regulation of Th17 cell response, which was partly dependent on adenosine receptor A1 and A3 subtypes, but up-regulation of allergen-specific IL-13 production from T cells. Lung inflammation induced by LPS-containing allergen was markedly reduced in IL-13-deficient mice in the context of ASA treatment, but not without ASA. Meanwhile, adenosine levels in the lung were enhanced by ASA treatment. Moreover, lung infiltration of eosinophils induced by ASA treatment was reversed by co-treatment of a xanthine oxidase inhibitor (allopurinol). Conclusion:, These findings suggest that ASA changes Th17-type into Th2-type inflammation mainly via the adenosine and uric acid metabolic pathway in the lung. [source]

A rapid TLC autographic method for the detection of xanthine oxidase inhibitors and superoxide scavengers

PHYTOCHEMICAL ANALYSIS, Issue 1 2006
I. Ayelen Ramallo
Abstract A new bioautographic assay suitable for the localization of xanthine oxidase inhibitors and superoxide radical scavengers present in a complex matrix is described. Enzyme activity is detected by reaction of superoxide radicals with nitroblue tetrazolium to form a blue formazan salt. Both activities can be differentiated using a non-enzymatic version of the autographic assay wherein superoxide is chemically generated. Copyright © 2005 John Wiley & Sons, Ltd. [source]