Abstract

The detailed mechanism and pathological changes of Alzheimer's disease (AD) are not clear as yet. Treated drugs of AD are limited and the effects of them on AD patients are not satisfied. So there is an urgent need for the development of drugs that can ameliorate or delay the onset of symptoms of the disease. Aim of the research is to investigate learning-memory function and pahtological changes related with β-amyloid (Aβ) in brains of APP transgenic (Tg) mice, and to observe the protective effects of Icarrin (ICA), a component of Traditional Chinese Medicine (TCM)_Epimedium, on above-mentioned targets and the expression of α-synuclein which is the precursor protein of non β-amyloid component (NAC) in brains of APP Tg mice. The mice of drug treated group were administered introgastrically by ICA (at doses 18 and 58 mg/kg/d) from 4 to 10 months old. The mice of normal group and negative transgene group were administered of distilled water by the same way. The learning-memory ability as measured by applying Morris water maze (MWM). The expression of APP, β-secretase (BACE), and the expression of α-synuclein in brains were detected by immunohistochemistry and western blot respectively. The content of βamyloid 1–42 (Aβ1–42) were measured by ELISA Assay. The amyloid senile plaques were detected by Congo red staining. The results showed that the escape latency and swimming distance in MWM of APP Tg mice were prolonged. The expression of APP, BACE, the content of Aβ1–42 decreased, the amount of amyloid senile plaques and the expression of α-synuclein increased in brains of APP Tg mice. ICA decreased the latency and swimming distance in MWM test, decreased the expression of APP, BACE in both hippocampus and cortex and the content of Aβ1–42 in hippocampus of model mice, and relieved amyloid plaques burden in brains of model mice. Meanwhile, ICA suppressed the expression of α- synuclein. These results suggest that APP Tg mice could mimic pathological proceedings of AD. Icarrin may have a promising application prospect in treatment of AD.

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