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

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.