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The protective effect of frusemide on the generation of superoxide anions by human bronchial epithelial cells and pulmonary macrophages in vitro
Affiliation:1. Department of Critical Care Medicine, University of Alberta, Edmonton, AB, Canada;2. Research Facilitation, Analytics (DIMR), Alberta Health Services, Edmonton, AB, Canada;3. Department of Nephrology, University of Toronto, Toronto, ON, Canada;4. Li Ka Shing Knowledge Institute, St. Michael''s Hospital, Toronto, ON, Canada;5. Department of Medicine, Medical University of South Carolina, Charleston, SC, USA;6. Department of Nephrology, University of California San Francisco, San Francisco, CA, USA;7. Section of Nephrology Department of Medicine, University of Chicago, Chicago, IL, USA;8. Department of Medicine, University of California - San Diego, San Diego, CA, USA
Abstract:Inhaled frusemide has been shown to inhibit bronchoconstriction induced by immunological and nonimmunological stimuli in asthmatic patients. The mechanisms by which this compound exerts its effect in asthmatic airways are unknown, but an inhibitory action on the activation of inflammatory cells or on the responsiveness of sensory epithelial nerves may be involved.In this study, we give evidence that frusemide prevents in part the activation of bronchial epithelial cells and pulmonary macrophages, as it reduces the rate of superoxide anion generation induced by IgE receptor crosslinking and by phorbol myristate acetate by 40–60%. The effect was not specific since we used stimuli which activate different signal transduction pathways for NADPH oxidase stimulation and frusemide was equally effective.
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