Cabergoline prevents necrotic neuronal death in an in vitro model of oxidative stress

Eur J Pharmacol. 2002 Dec 20;457(2-3):95-8. doi: 10.1016/s0014-2999(02)02683-3.

Abstract

To study if cabergoline, a long-lasting specific dopamine D2 receptor agonist, has neuroprotective effects against oxidative stress, we exposed (3 h) SH-SY5Y human neuroblastoma cells to tert-butylhydroperoxide (t-BOOH; 500 microM). t-BOOH caused a 42+/-4% neuronal death, which was prevented by cabergoline (2 h before) in a concentration-dependent manner (EC(50): 1.24 microM). This effect was not antagonised by haloperidol (concentration up to 10 microM), and was associated with an increased availability of intracellular GSH contents (+30+/-11%) and a decrease in the membrane lipid peroxidation (-23+/-9%). Our data suggest that cabergoline has neuroprotective effects useful for Parkinson's disease therapy.

MeSH terms

  • Cabergoline
  • Cell Death / drug effects
  • Cell Survival / drug effects
  • Dopamine Agonists / pharmacology*
  • Dopamine Antagonists / pharmacology
  • Dopamine D2 Receptor Antagonists
  • Dose-Response Relationship, Drug
  • Ergolines / pharmacology*
  • Free Radicals / metabolism
  • Haloperidol / pharmacology
  • Humans
  • Lipid Peroxidation / drug effects
  • Models, Neurological
  • Necrosis
  • Neurons / drug effects*
  • Neurons / pathology
  • Neuroprotective Agents / pharmacology*
  • Oxidative Stress / drug effects*
  • Parkinson Disease / metabolism
  • Parkinson Disease / prevention & control
  • Receptors, Dopamine D2 / agonists
  • Tumor Cells, Cultured
  • tert-Butylhydroperoxide / toxicity

Substances

  • Dopamine Agonists
  • Dopamine Antagonists
  • Dopamine D2 Receptor Antagonists
  • Ergolines
  • Free Radicals
  • Neuroprotective Agents
  • Receptors, Dopamine D2
  • tert-Butylhydroperoxide
  • Haloperidol
  • Cabergoline