Objective:　Vincamine　is　a　plant　alkaloid　used　clinically　as　a　peripheral　vasodilator　that　increases　cerebral　blood　flow　and　oxygen　and　glucose　utilization　by　neural　tissue　to　combat　the　effect　of　aging.　The　main　purpose　of　the　present　study　is　to　investigate　the　influence　of　vincamine　on　amyloid-P　25-35　(A　beta　25-35)　induced　cytotoxicity,　to　gain　a　better　understanding　of　the　neuroprotective　effects　of　this　clinically　used　anti-Alzheimer＇s　disease　drug.　Materials　and　Methods:　Oxidative　stress　was　assessed　by　measuring　malondialdehyde,　glutathione,　and　superoxide　dismutase　(SOD)　levels.　Cell　viability　was　assessed　by　3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium　bromide　assay.　Cell　apoptosis　detection　was　performed　using　an　Annexin-V-FITC　Apoptosis　Detection　Kit.　The　production　of　reactive　oxygen　species　(ROS)　was　determined　using　an　ROS　Assay　Kit.　Western　blot　detection　was　carried　out　to　detect　the　protein　expression.　Results:　Our　studies　showed　that　pretreatment　with　vincamine　could　reduce　A　beta　25-35　induced　oxidative　stress.　Vincamine　markedly　inhibited　cell　apoptosis　dose-dependently.　More　importantly,　vincamine　increased　the　phosphatidylinositol-3　kinase　(PI3K)/Akt　and　Bcl-2　family　protein　ratios　on　preincubation　with　cells　for　2　h.　Conclusion:　Above　observation　led　us　to　assume　that　one　possible　mechanism　of　vincamine　protects　A　beta　25-35-induced　cell　death　could　be　through　upregulation　of　SOD　and　activation　of　the　PI3K/Akt　pathway.