Regulation of cyclooxygenase-2 expression in human osteoblastic cells by N-acetylcysteine

J Lab Clin Med. 2000 Nov;136(5):390-4. doi: 10.1067/mlc.2000.110369.


Cyclooxygenase (COX) plays a pivotal role in the inflammatory process of inflammatory arthropathies. Inflammatory cytokines induce COX-2 expression in osteoblasts of inflamed joints, followed by osteoclast activation. The inhibition of COX-2 expression could help prevent prostaglandin E2 secretion, followed by osteoclast activation for bone destruction and resorption. We examined whether the antioxidant N-acetylcysteine (NAC) inhibited COX-2 expression induced in the human osteoblastic cell line MG63 by interleukin-1beta (IL-1beta). According to Western blot and reverse transcription-polymerase chain reaction (RT-PCR) test results, NAC inhibited IL-1beta-induced COX-2 expression in protein and messenger RNA. We also demonstrated immunohistochemically that NAC inhibited NFkappaB nuclear translocation. These results suggested that NAC inhibited both COX-2 expression and NFkappaB nuclear translocation in MG63, which in turn indicated that NAC could inhibit the inflammatory process involved in bone resorption by regulating COX-2 expression at the level of transcription.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcysteine / pharmacology*
  • Animals
  • Cell Line
  • Cyclooxygenase 2
  • Gene Expression Regulation, Enzymologic / drug effects*
  • Humans
  • Interleukin-1 / pharmacology
  • Isoenzymes / genetics*
  • Membrane Proteins
  • NF-kappa B / metabolism
  • Osteoblasts / metabolism*
  • Prostaglandin-Endoperoxide Synthases / genetics*
  • Rabbits


  • Interleukin-1
  • Isoenzymes
  • Membrane Proteins
  • NF-kappa B
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Prostaglandin-Endoperoxide Synthases
  • Acetylcysteine