We also assume that the modulation of the brain cortex cells ' redox status sufficiently contributes to 3 - EA protective property . Monoamine oxidase A and B ( Mao - A and Mao - B ) degrade amines and are also a source of mitochondrial ROS [ 27,28 ] . Moreover , Mao - A is expressed at a high level in neurons , whereas Mao - B is expressed in astrocytes [ 29,30 ] . Mao inhibitors prevent dopamine - induced mPTP pore formation and cell death [ 31 ] . Catalase is a key enzyme in brain cells that utilizes ROS during ischemia and reoxygenation [ 32 ] . Its overexpression in brain cells before MCA occlusion has a powerful protective effect , while this approach is not effective in the therapeutic regimen [ 33 ] . In our experiments , the incubation of cerebral cortex cells with 3 - EA lead to the suppression of basal and OGD / Rinduced expression of genes encoding both forms of monoamine oxidase ; the protective effect of 3 - EA is observed both in neurons and astrocytes . As for the gene encoding catalase , its baseline expression increased almost threefold after pretreatment of cells with 3 - EA . The increased level of catalase persisted after OGD / R. Our in vitro results are supported by the data obtained in animal experiments . Daily intravenous administration of 18.0 mg / kg 3 - EA during a week following MCA occlusion ameliorates the severity of the neurological disorder and preserves neurons ' cellular population and brain tissue integrity . In addition , restraining the activity of local oxidative stress and simultaneous prevention of ischemia - induced AC 's drastic depression highlights the importance of the antioxidant property of the novel hydroxypyridine compound .