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Background  The aim of the present study was to investigate the effects of  Scutellaria barbata  flavonoids (SBF) on memory impairment and neuronal injury induced by amyloid beta protein 25–35 in combination with aluminum trichloride (AlCl3) and recombinant human transforming growth factor-β1 (RHTGF-β1) (composited Aβ) in rats.    Methods  The composited Aβ-treated model of Alzheimer’s disease (AD)-like memory impairment and neuronal injury was established in male rats by right intracerebroventricular injection of composited Aβ, and the effects of SBF were assessed using this rat model. Spatial learning and memory of rats were assessed in the Morris water maze, and neuronal injury was assessed by light and electron microscopy with hematoxylin-eosin or uranyl acetate and lead nitrate-sodium citrate staining, respectively.    Results  In the Morris water maze, memory impairment was observed in 94.7% of the composited Aβ-treated rats. The composited Aβ-treated rats took longer than sham-operated rats to find the hidden platform during position navigation and reversal learning trials. They also spent less time swimming in the target quadrant in the probe trial. Optical and electron microscopic observations showed significant neuropathological changes including neuron loss or pyknosis in hippocampus, typical colliquative necrosis in cerebral cortex, mitochondrial swelling and cristae fragmentation and a large number of lipofuscin deposits in the cytoplasm. Treatment with SBF (35–140 mg/kg) reduced the memory impairment and neuronal injury induced by composited Aβ.    Conclusion  SBF-mediated improvement of composited Aβ-induced memory impairment and neuronal injury in rats provides an appropriate rationale for evaluating SBF as a promising agent for treatment of AD.    Electronic supplementary material  The online version of this article (doi:10.1186/s12993-016-0118-8) contains supplementary material, which is available to authorized users.

Scutellaria barbata flavonoids alleviate memory deficits and neuronal injuries induced by composited Aβ in rats