Objective To observe the influence of XueShuanXinMaiNing(XSXMN)in the behavior and structures of cerebral cortex and hippocampus of the rats withβamyloid protein(Aβ)-induced Alzheimer’s disease(AD),and to explore its therapeutic effects on the rat AD.Methods 100 male Wistar rats were selected.According to weight, the rats were randomly divided into sham operation group, model group, positive drug group (donepezil hydrochloride,1.75 mg· kg-1 ),XSXMN 1.1 g· kg-1 group and XSXMN 2.2 g· kg-1 group. The rat AD models were made by injecting Aβinto hippocampus.After oral administration for 15 d,Morris water maze test, dark avoidance task and pathology test were performed.Results In Morris water maze test,compared with model group,the latency and swimming distance to platform of the rats in XSXMN 1.1 g·kg-1 group were decreased on the 2nd,4th and 5th day(P<0.05 or P<0.01);in XSXMN 2.2 g·kg-1 group,the latency to platform of the rats were decreased from the 3nd to 6th day(P<0.05 or P<0.01),the swimming distances to platform of the rats were decreased from the 3rd to 5th day(P<0.05 or P<0.01).On the 7th day,in XSXMN groups,the times of passing platform,time of staying on platform,distance of staying on platform,time of staying in effective area, distance of staying in effective area, time of staying on platform/total time, distance of staying on platform/total distance,time of staying on platform/total time were all increased significantly(P<0.05 or P<0.01)within 90 s. In dark avoidance task,compared with model group,the error latency and the error times of the rats in XSXMN groups had no obvious change on the 2nd day.The pathological results showed that there were degeneration nerve cells and necrosis nerve cells in the rat cerebral cortex in XSXMN groups,while in the rat hippocampus there were less number of nerve cells with obscure cell layer and many degeneration and necrosis cells were found;compared with model group,there was no obvious improvement.Conclusion XSXMN can improve the learning and memory function of the AD rats.