Inhibitory action of minocycline on lipopolysaccharide-induced release of nitric oxide and prostaglandin E2 in BV2 microglial cells

Arch Pharm Res. 2004 Mar;27(3):314-8. doi: 10.1007/BF02980066.


Microglia are the major inflammatory cells in the central nervous system and become activated in response to brain injuries such as ischemia, trauma, and neurodegenerative diseases including Alzheimer's disease (AD). Moreover, activated microglia are known to release a variety of proinflammatory cytokines and oxidants such as nitric oxide (NO). Minocycline is a semisynthetic second-generation tetracycline that exerts anti-inflammatory effects that are completely distinct form its antimicrobial action. In this study, the inhibitory effects of minocycline on NO and prostaglandin E2 (PGE2) release was examined in lipopolysaccharides (LPS)-challenged BV2 murine microglial cells. Further, effects of minocycline on inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression levels were also determined. The results showed that minocycline significantly inhibited NO and PGE2 production and iNOS and COX-2 expression in BV2 microglial cells. These findings suggest that minocycline should be evaluated as potential therapeutic agent for various pathological conditions due to the excessive activation of microglia.

MeSH terms

  • Animals
  • Cell Line
  • Dinoprostone / antagonists & inhibitors
  • Dinoprostone / metabolism*
  • Lipopolysaccharides / antagonists & inhibitors
  • Lipopolysaccharides / pharmacology*
  • Mice
  • Microglia / drug effects*
  • Microglia / metabolism
  • Minocycline / pharmacology*
  • Nitric Oxide / antagonists & inhibitors*
  • Nitric Oxide / metabolism*


  • Lipopolysaccharides
  • Nitric Oxide
  • Minocycline
  • Dinoprostone