Nonsteroidal antiinflammatory drugs: Effects on normal and interleukin 1 treated human articular chondrocyte metabolism in vitro

R. L. Smith, G. Kajiyama, Nancy E Lane

Research output: Contribution to journalArticle

35 Scopus citations

Abstract

Objective. To test the effects of nonsteroidal antiinflammatory drugs (NSAID), naproxen, ibuprofen and diclofenac, and salicylates on normal and interleukin 1 (IL-1) treated human articular chondrocyte metabolism in vitro. Methods. Normal adult human articular chondrocytes were isolated and cultured as primary monolayers; the cells were treated with NSAID and salicylates at low and high plating density for assessing effects on proliferation and matrix synthesis and IL-1 modulated cell metabolism, respectively. Results. Cell proliferation was inhibited by ibuprofen and high doses of salicylates. Glycosaminoglycan (GAG) synthesis was stimulated by ibuprofen at 10 μg/ml but was not changed by any other drugs at similarly low concentrations; at medium to high concentrations, only the salicylates inhibited GAG synthesis. Collagen synthesis was unaffected by any drug at the concentrations tested. IL-1 induced prostaglandin E2 release was completely inhibited by the NSAID and partially inhibited by the salicylates. IL-1 induced IL-6 release was inhibited by ibuprofen and the salicylates whereas IL-1 induced APMA-activated collagenase was only inhibited by the salicylates. Conclusion. Normal human chondrocytes respond differentially to naproxen, ibuprofen, diclofenac, and the salicylates; these observations suggest that each drug may exhibit unique attributes with respect to longterm efficacy on cartilage metabolism.

Original languageEnglish (US)
Pages (from-to)1130-1137
Number of pages8
JournalJournal of Rheumatology
Volume22
Issue number6
StatePublished - 1995
Externally publishedYes

Keywords

  • collagenase
  • extracellular matrix
  • human articular cartilage
  • interleukin 1
  • interleukin 6
  • nonsteroidal antiinflammatory drugs

ASJC Scopus subject areas

  • Immunology
  • Rheumatology

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