Abstract: AimTo study the effects of 9-(4-ethoxycarbonylphenoxy)-6,7-dimethoxy-1,2,3,4-tetrahydro acridine (EDT) on free radical induced injury in primary cultured rat cortical neuron and cerebral ischemia in mice. MethodsIn primary rat cortical neuron, free radical injury model was established by 10 μmol·L^-1 H₂O₂. The content of malondiadehyde (MDA) and activity of superoxide dismutase (SOD) in cells were investigated. Chronic cerebral ischemia model was produced by occlusion of one carotid artery and pneumogastric nerve in mice. The step down test was adopted to investigate the effect of EDT on the memory impairment. The cerebra morphology and MDA, NO content and SOD activity in mice cerebra were detected. ResultsIn primary rat cortical culture, 0.01-3 μmol·L^-1 EDT concentration-dependently inhibited the formation of MDA and reduction of SOD activity induced by 10 μmol·L^-1 H₂O₂. In chronic cerebral ischemia, EDT 2.5, 5 and 10 mg·kg^-1 ig for 5 d greatly improved the memory impairment, reduced NO efflux and MDA content, while increased SOD activity in mice cerebra. ConclusionEDT was found to protect neurons from H₂O₂-induced neurotoxicity and inhibit chronic cerebral ischemia mediated injury and memory impairment in mice.