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, Volume 21, Issue 1–2, pp 121–129 | Cite as

Inhibition of neutrophil oxidative metabolism by nimesulide

  • F. Capsoni
  • E. Venegoni
  • F. Minonzio
  • A. M. Ongari
  • V. Maresca
  • C. Zanussi
Immunosuppression and Inflammation

Abstract

Oxygen derived free radical release from activated neutrophils may be in part responsible of tissue damage in the acute phase of inflammation. We have shown that the methane sulfonanilide antiinflammatory agent nimesulide inhibits the respiratory burst of phagocytosing neutrophils without affecting their phagocytic or chemotactic responsiveness. In fact, chemiluminescence and superoxide anion generation by polymorphonuclear leukocytes (PMN) stimulated with zymosan particles or with the synthetic peptide FMLP are inhibited by nimesulide and its 4-OH metabolite in a dose dependent fashion without affecting cell viability. The control of the extracellular flux of radical species by phamacological compounds may affect the course of inflammation reducing tissue damage. Our data suggest that the inhibition of superoxide anion production by neutrophils is an additional mechanism of action of the antiinflammatory agent nimesulide.

Keywords

Synthetic Peptide Oxidative Metabolism Nimesulide Polymorphonuclear Leukocyte Superoxide Anion Production 

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Copyright information

© Birkhäuser Verlag 1987

Authors and Affiliations

  • F. Capsoni
    • 1
  • E. Venegoni
    • 1
  • F. Minonzio
    • 1
  • A. M. Ongari
    • 1
  • V. Maresca
    • 2
  • C. Zanussi
    • 1
  1. 1.Istituto di Clinica Medica IIUniversitàBalsamo (MI)
  2. 2.LPB Istituto FrarmaceuticoS.P.A. di CiniselloBalsamo (MI)

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