The Effect of Some Anti‐inflammatory Agents on Elastase Release From Neutrophils In‐vitro
Identifieur interne : 003055 ( Main/Exploration ); précédent : 003054; suivant : 003056The Effect of Some Anti‐inflammatory Agents on Elastase Release From Neutrophils In‐vitro
Auteurs : E. O. Adeyemi [Royaume-Uni] ; V. S. Chadwick [Royaume-Uni] ; H. J. F. Hodgson [Royaume-Uni]Source :
- Journal of Pharmacy and Pharmacology [ 0022-3573 ] ; 1990-07.
English descriptors
- Teeft :
- Acetylsalicylic acid, Adeyemi, Arachidonic acid metabolism, Assay, Connective tissue, Dark bars, Ducane road, Elastase, Elastase assay buffer, Elastase release, Elastase secretion, Enzyme activity, Febs lett, Functional assay, Functional inhibition, Human leucocyte elastase, Indomethacin, Inflammatory, Inflammatory bowel disease, Inhibitory capacity, Klotz maier, Leucocyte, Leucocyte elastase, Lipoxygenase pathway, Maximum elastase activity, Nast leduc, Neutrophil, Neutrophil elastase, Neutrophil elastase release, Pathway, Percentage decrease, Polymorphonuclear leucocytes, Positive control, Prednisolone, Radioimmunometric assay, Radiolabelled protein, Rheumatoid arthritis, Room temperature, Salicylic acid, Short preincubation period, Sigma chemicals, Sodium azide, Sulphosalicylic acid, Supernatant, Tissue damage, Ulcerative colitis, Various concentrations, West germany.
Abstract
Abstract— In view of the potential role of released polymorphonuclear leucocyte elastase in causing tissue damage, the effect of commonly used anti‐inflammatory drugs on elastase release from neutrophils has been studied in‐vitro. Elastase release from neutrophils exposed to the synthetic bacterial cell wall peptide N‐formyl‐L‐methionyl‐L‐leucyl‐L‐phenylalanine (10−6 M) was quantitated using a radiometric immunoassay and a functional assay of elastase. Prednisolone and non‐steroidal anti‐inflammatory drugs inhibited elastase release at concentrations from 0.1 mM‐0.1 nM. No inhibition by sulphosalicylic acid, D‐penicillamine or chloroquine sulphate was observed. The clinical relevance of these findings is discussed.
Url:
DOI: 10.1111/j.2042-7158.1990.tb06601.x
Affiliations:
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<term>Connective tissue</term>
<term>Dark bars</term>
<term>Ducane road</term>
<term>Elastase</term>
<term>Elastase assay buffer</term>
<term>Elastase release</term>
<term>Elastase secretion</term>
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<term>Febs lett</term>
<term>Functional assay</term>
<term>Functional inhibition</term>
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<term>Inhibitory capacity</term>
<term>Klotz maier</term>
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<term>Leucocyte elastase</term>
<term>Lipoxygenase pathway</term>
<term>Maximum elastase activity</term>
<term>Nast leduc</term>
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<term>Neutrophil elastase</term>
<term>Neutrophil elastase release</term>
<term>Pathway</term>
<term>Percentage decrease</term>
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<term>Positive control</term>
<term>Prednisolone</term>
<term>Radioimmunometric assay</term>
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<term>Salicylic acid</term>
<term>Short preincubation period</term>
<term>Sigma chemicals</term>
<term>Sodium azide</term>
<term>Sulphosalicylic acid</term>
<term>Supernatant</term>
<term>Tissue damage</term>
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<term>Various concentrations</term>
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<front><div type="abstract" xml:lang="en">Abstract— In view of the potential role of released polymorphonuclear leucocyte elastase in causing tissue damage, the effect of commonly used anti‐inflammatory drugs on elastase release from neutrophils has been studied in‐vitro. Elastase release from neutrophils exposed to the synthetic bacterial cell wall peptide N‐formyl‐L‐methionyl‐L‐leucyl‐L‐phenylalanine (10−6 M) was quantitated using a radiometric immunoassay and a functional assay of elastase. Prednisolone and non‐steroidal anti‐inflammatory drugs inhibited elastase release at concentrations from 0.1 mM‐0.1 nM. No inhibition by sulphosalicylic acid, D‐penicillamine or chloroquine sulphate was observed. The clinical relevance of these findings is discussed.</div>
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