Objective To explore the effect oftroxerutin on β-amyloid(Aβ25-35)-induced AD models,and provide experimental evidence for AD drug development.Methods Fifty SD rats were randomly divided into 5 groups(n=10),namely,normal control group,model group,and low-,mediumand high-dose troxerutin treatment groups.Rats of the normal control group and model group were given sodium carboxymethylcellu lose,and intragastric administration oftroxerutin(10,20 and 50 mg/kg,respectively)was performed on rats of the low-,medium- and high-dose troxerutin treatment groups.Fourteen d after administration of troxerutin,Aβ25-35 at a dosage of 1 μL was injected into the bilateral hippocampus areas of rats in the model group and 3 treatment groups,while rats of the normal control group was not given any treatment.Open field test was employed to detect the motor function changes,and Y-maze test was employed to observe the cognitive function changes; activities of choline acetyltransferase(ChAT) and acetylcholinesterase(AChE) in the hippocampus areas of rats were measured by colorimetric method,and expressions of Bcl and Bax were detected by Western blotting.Results In the open field,the scores of vertical motion in the medium- and high-dose troxerutin treatment groups were significantly higher than those in the model group(P＜0.05); in the Y-maze test,the frequency of correct responses in the medium- and high-dose troxerutin treatment groups was significantly increased as compared with that in the model group(P＜0.05).As compared with that in the model group,the activity of ChAT in the high-dose troxerutin treatment group was obviously increased (P＜0.05); no significant difference on the activity of AchE was noted between each 2 groups(P＞0.05).The expression of Bcl was statistically increased and that of Bax was obviously decreased in the mediumand high-dose troxerutin treatment groups as compared with those in the model group (P＜0.05).Conclusion Troxerutin has a protective effect on Aβ25-35-induced neurotoxicity,whose mechanism may be related to the increase of ChAT activity.