Heavy ethanol consumption aggravates the ischemic cerebral injury by inhibiting ALDH2

BACKGROUND: Heavy ethanol consumption is widely accepted as a risk for ischemic stroke. The molecular mechanisms of ethanol-induced brain injury have not been fully understood. AIM: This study aims to find out the mechanism of the ischemic cerebral injury. METHODS: We used Sprague-Dawley rats with transient middle cerebral artery occlusion for acute experiment and stroke-prone spontaneously hypertensive rats for long-term experiment in vivo, and oxygen-glucose deprivation model in vitro to define a detrimental effect of different doses of ethanol on ischemic stroke injury. We also used mitochondrial aldehyde dehydrogenase 2 knockdown/overexpression or inhibitor/activator to investigate mechanism of the adverse effects of ethanol. RESULTS: High-dose ethanol (36% of calorie derived from ethanol) significantly increased the infarct size in rats (P CONCLUSIONS: High concentrations of ethanol aggravate cerebral injury by inhibiting of aldehyde dehydrogenase 2 and inducing excess accumulation of aldehydes. Language: en