Ethanol attenuates ischemic and hypoxic injury in rat brain and cultured neurons

Neuroreport. 2003 Nov 14;14(16):2089-94. doi: 10.1097/00001756-200311140-00016.

Abstract

Reactive oxygen species play a critical role in ischemic injury and oxidative stress induces apoptosis and triggers inflammation in neural cells. The effect of ethanol on ischemic brain injury was examined. Ethanol attenuated ischemia/reperfusion-induced brain infarction and elevation of inflammatory mediators, including tumor necrosis factor-alpha (TNF-alpha) expression, metalloproteinase-9, and neutrophil-associated myeloperoxidase activities. In cultured neurons, ethanol suppressed combined oxygen and glucose deprivation (COGD)/reoxygenation-induced oxidative stress and neuronal apoptosis. Furthermore, ethanol suppressed COGD/reoxygenation-induced activation of NF-kappaB, a free-radical-sensitive regulator, leading to the attenuation of TNF-alpha expression in glial cultures. We propose that scavenging of free radicals and attenuation of free-radical-induced alterations might account for ethanol's beneficial action against ischemic brain injury.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Apoptosis / physiology
  • Brain / drug effects*
  • Brain / metabolism
  • Brain / pathology
  • Brain Infarction / drug therapy
  • Brain Infarction / metabolism
  • Brain Infarction / physiopathology
  • Cells, Cultured
  • Down-Regulation / drug effects
  • Down-Regulation / physiology
  • Encephalitis / drug therapy
  • Encephalitis / metabolism
  • Encephalitis / physiopathology
  • Ethanol / pharmacology*
  • Ethanol / therapeutic use
  • Free Radical Scavengers / pharmacology
  • Free Radical Scavengers / therapeutic use
  • Free Radicals / antagonists & inhibitors
  • Free Radicals / metabolism
  • Hypoxia-Ischemia, Brain / drug therapy*
  • Hypoxia-Ischemia, Brain / metabolism
  • Hypoxia-Ischemia, Brain / pathology
  • Inflammation Mediators / antagonists & inhibitors
  • Inflammation Mediators / metabolism
  • Male
  • NF-kappa B / drug effects
  • NF-kappa B / metabolism
  • Neurons / drug effects*
  • Neurons / metabolism
  • Neurons / pathology
  • Neuroprotective Agents / pharmacology
  • Neuroprotective Agents / therapeutic use
  • Oxidative Stress / drug effects
  • Oxidative Stress / physiology
  • Rats
  • Rats, Sprague-Dawley
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Free Radical Scavengers
  • Free Radicals
  • Inflammation Mediators
  • NF-kappa B
  • Neuroprotective Agents
  • Tumor Necrosis Factor-alpha
  • Ethanol