This research was designed to investigate the pharmacological effects of aconitine on attenuating neuronal damage induced by amyloid β protein fragment 1-40 (Aβ_1-40) via inhibition of glycogen synthase kinase-3β (GSK-3β).Based on cell safety tests,5 nmol/L was set as the appropriate concentration of aconitine used in following experiments.A cell-damage model was established by incubating SH-SY5Y cells with Aβ_1-40 (20 μmol/L) for 24 hours.3 experimental groups were set up:the normal control,Aβ_1-40-damaged cell model control and aconitine-treated group,while the last group was pre-treated with aconitine (5 nmol/L) for 12 hours.The lactate dehydrogenase (LDH) in cell culture supernatant was measured using ELISA.The apoptosis and necrosis were analyzed by flow cytometry.The cell GSK-3β protein phosphorylation was detected by Western blotting.Compared with the Model,the significantly lower LDH in cell culture supernatant,cell apoptosis or necrosis rate and phosphorylated GSK-3β levels were detected in the aconitine-treated group.These data suggested that aconitine can substantially alleviate the neuronal damage caused by Aβ_1-40,and the benefit may be related to the inhibition of GSK-3β hyper-phosphorylation by aconitine.