Berberine attenuates cognitive deficits via improving NGF signaling in AD mice
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Graphical Abstract
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Abstract
ObjectiveTo investigate the change of nerve growth factor(NGF) signaling and mechanisms of berberine on learning and memory deficits in Alzheimer's disease(AD) mice.MethodsWe adopted APP/PS1 mice as AD animal model; we used Y maze to measure learning and memory function and Western blot to investigate the protein expression levels.ResultsCompared with the control mice(77.57±11.81),the APP/PS1 mice exhibited reduced spontaneous alternation behavior(55.71±12.33)(P<0.01).Berberine(30 mg/kg) attenuate the impairment of spontaneous alternation behavior(70.93±15.99)(P<0.01).The expression levels of NGF,tyrosine kinases(TrkA),phosphorylated extracellular regulated protein kinases(p-ERK),and phosphorylated cAMP-response element binding protein(p-CREB) in the hippocampus were lower in APP/PS1 mice compared to those of the control mice(P<0.05),but were higher in the berberine(30 mg/kg) treated mice compared to those of the APP/PS1 mice(P<0.05).ConclusionBerberine attenuates learning and memory impairments in APP/PS1 mice,possibly through the NGF signaling pathway.
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