Improved neurological deficits and reduced brain infarction volume, neuronal apoptotic cell death accompanied by up-regulation of Bcl-2 and down-regulation of Bax and caspase-3. Reduced oxidative stress (counteracted lipid peroxidation and restored glutathione content and superoxide dismutase activity) in the cerebral cortex. The gene discussed is CASP3; the disease is brain infarction.