Objective: To establish the model of impaired memory and neurologic damaged by intracerebroventricular injection of amyloid beta protein 25-35 in combination with AlCl3 and RHTGF-β1 (composited Aβ) in rats and detect the effects of Scutellaria barbata flavonoids (SBF) with this model. Methods: Male SD rats were received intracere- broventricular injection of RHTGF-β1 on the day 1 of operation, and then intracerebroventricularly injected Aβ 25-35 for consecutive 14 d in every morning and AlCl3 for consecutive 5 d in every afternoon from the day 2 of operation. Sham control rats were conducted the same operation, but intracerebroventricularly injected the equal volume saline. On the day 45 of operation, all rats were performed the Morris water maze training for succeSBFul memory impairment model screening. The swimming scores of every operated rat and sham control rats on the day 4 of water maze training were used for calculating the successful model screening ratio (SR). When SR of any rat was more than 0.2, the rat was confirmed to be a succeSBFul model rat. On the day 49 of operation, all successful model rats were randomly divided into 4 groups, model control and 3 doses of SBF group rats. The SBF group rats were administered 35, 70 and 140 mg/kg SBF for 38 d, and model control and sham control rats were given an equal volume of saline. On the day 31 administered of drug that is on the day 79 operation, all the rats were carried out the consecutive 7 d Morris water maze task for memory ability detection. The positioning navigation task on the day 1 and 2 of Morris water maze training was used to evaluate the rats’ memory acquirement, the probe trial on the day 3 of Morris water maze was used to detect the memory retention, the reversal trial on the day of 4, 5 and 6 of Morris water maze was used to evaluate the rats’ memory reproducibility and visible platform trial was used to test the rats’ swimming speed. On the second day of the last water maze task, that was the 86 d after operation, all the rats were decapitated, the microanatomy of brain was observed with naked eye and the morphologic structure/substructure of neuron were examined with light/electron microscope by hematoxylin-eosin (HE)/thiamine or uranyl acetate and lead nitrate–sodium citrate staining, respectively. Results: In the 4 d successful model rats’ screening by Morris water maze task, the time taken in finding the hidden platform (latency) progressively declined in all rats. The successful rate of memory impairment model in the present study was 94.70%. In the positioning navigation trial model rats always took longer latency to find the hidden platform on the day 1 and 2 test in the water maze task, as compared with the sham control (P<0.01). However, SBF can significantly shorten the time to reach the platform as compared with model rats (P <0.01). In the probe trial, the model rats took decreased time, distance and crossing number in target quadrant (the first quadrant) within 60 s, as compared with sham control rats (P<0.01). While the three dose of SBF at 35, 70 and 140 mg/kg exert differently attenuated the above decreases in swimming time, swimming distance and crossing number of model control rats in target quadrant(P<0.05, P<0.01). In the reversal trial, the modell rats always spent longer time to find the hidden platform on the day 4, 5 and 6 of Morris water maze test (P<0.01). Interestingly, SBF 35, 70 and 140 mg/kg can significantly shorten latency onto the platform of model control rats (P<0.05, P<0.01). In the visible platform test, that was the 7th Morris water maze training, the time of all rats in each group spent to reach the visible platform was no significantly difference. The result indicated that swimming speed of each group rats were approximate in water maze, which may eliminate disturbance of swimming score as their swimming speed discrepancy. On the 86 d of operation with naked viewed, the brain in model rats appeared lessened weight of brain, yellow surface of cerebral cortex, and cortical thinned or collapsed in some rats. The neuron of hippocampus and cerebral cortex was found a markedly pathological change by HE and thionine staining under light microscope observation, such as neuron loss, cell swelling and Nissl bodies decrease. Some neuron of cerebral cortex in model control rats occurred typical colliquative necrosis, including cell membrane broken, nucleus dissolved and a great inflammatory cell infiltrated in necrosis region. Electron microscopy found that the hippocampus neuron pyknosis, nuclear membrane pit, nucleolus margination, chromatin condensation, ribosome separation in cytoplasm, a large lipofuscin deposition, mitochondria swelling, endoplasmic reticulum expansion, astrocyte foot processes edema, myelin sheath lamellar damage, axon and myelinated nerve loss, a large excitatory neurotransmitter at presynaptic membrane. However, different dose of SBF by administration for 38 d differently reversed the above neuronal pathological changes induced by composited Aβ25-35 which the neuron and Nissl body count increase, the typical colliquative necrosis and subcellular structure damages absents. Conclusion: Intracerebroventricular injection of composited Aβ can result in an impairment of memory and damages in neurostructure. Then, SBF was found that has markedly ameliorations on memory impaired and neuron damage.