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Cited by 64Phosphodiesterase function and regulationNeutrophil, Myeloperoxidase and Oxidative MechanismsInflammatory mediators and NSAID effects

The DOI matches its Crossref record; 58 of the 58 references it cites were found in a registry or an index.

Nimesulide decreases superoxide production by inhibiting phosphodiesterase type IV

Bevilacqua, Maurizio, Vago, Tarcisio, Baldi, Gabriella, Renesto, Elio, Dallegri, Franco, Norbiato, Guido·1994·European Journal of Pharmacology: Molecular Pharmacology
DOI 10.1016/0922-4106(94)90067-1
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Abstract

Nimesulide, the prototype of a new class of anti-inflammatory drugs, dose-dependently decreases the production of the superoxide anion (O2-.) in N-formyl-methionyl-leucyl-phenylalanine (fMLP)- and in phorbol myristate acetate (PMA)-stimulated polymorphonuclear leukocytes. The inhibition of O2-. is possibly related to its inhibitory effect on polymorphonuclear leukocyte cytosolic phosphodiesterase type IV (IC50 = 39 +/- 2 microM), to the related increase in cAMP (P < 0.01 at 1 microM) and the subsequent increase in protein kinase A activity. In fact H-89, a specific protein kinase A inhibitor, counteracts the inhibitory effect of nimesulide on O2-. production by fMLP and PMA. The activation of protein kinase A may prompt the phosphorylation of a number of substrates, thus inhibiting the assembly of NADPH-oxidase in the plasma membrane. Accordingly, nimesulide decreases PMA-induced assembly of NADPH-oxidase in polymorphonuclear leukocytes plasma membranes by about 35%. Protein kinase A activation may also interfere with chemotaxis. Nimesulide inhibits stimulated chemotaxis and the effect is decreased by H-89. Inhibition of phosphodiesterase type IV may explain many of nimesulide's effects.

Overview

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Registry

Crossref · 10.1016/0922-4106(94)90067-1

Cites

58 of 58 references verified0 citation errors · 0 not checkable

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Claims other papers make about this one

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  • These observations are confounded because nimesulide also inhibits phosphodiesterase (PDE) type IV, and PDE IV inhibitors, like rolipram, have been shown to enhance GR function.

    “these observations are somewhat confounded because nimesulide also inhibits phosphodiesterase (PDE) type IV, and PDE IV inhibitors, like rolipram, have been shown to enhance GR function (see below).70,71”

    From Cytokines and Glucocorticoid Receptor Signaling (2009) · cites this paper as [70]

Citations

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Research works printed but not linked: 1

  1. Davis, 1979, A simple direct assay of 3′, 5′-cyclic nucleotide phosphodiesterase activity based on the use of polyacrylamide-boronate affinity gel chromatography, J. Cyclic Nucleotide Res., 5, 65

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Metadata

Authors
Bevilacqua, M., Vago, T., Baldi, G., Renesto, E., Dallegri, F., & Norbiato, G.
Affiliations
Luigi Sacco Hospital (IT)
Corresponding author
Bevilacqua, Maurizio
ORCID
Venue
European Journal of Pharmacology: Molecular Pharmacology
Publisher
Elsevier BV
Published
1994-08
Volume
268
Issue
3
Pages
415-423
ISSN
0922-4106 (ISSN-L)
DOI
10.1016/0922-4106(94)90067-1
OpenAlex
W2005106478
Cited by
64
References
58
Citations by year
2023: 1 · 2019: 1 · 2018: 2 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 2 · 2012: 4
FWCI
1.00
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • European Journal of Pharmacology Molecular Pharmacology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Phosphodiesterase function and regulation
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Health Sciences › Medicine › Pharmacology (medical) › Inflammatory mediators and NSAID effects
Keywords
nimesulide, superoxide production, polymorphonuclear leukocytes, protein kinase A, cyclic AMP, leukocyte chemotaxis, fMLP stimulation, phorbol myristate acetate, anti-inflammatory agents
MeSH terms
Cyclic AMP, Adenylyl Cyclases, Anti-Inflammatory Agents, Non-Steroidal, Blood Platelets, Cell Membrane, Chemotaxis, Leukocyte, Humans, Isoquinolines, N-Formylmethionine Leucyl-Phenylalanine, NADH, NADPH Oxidoreductases, Neutrophils, Oxygen Consumption, Phosphodiesterase Inhibitors, Phosphoric Diester Hydrolases, Sulfonamides, Superoxides, Tetradecanoylphorbol Acetate, Protein Kinase Inhibitors, In Vitro Techniques

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