Abstract

Actinidia arguta (Actinidiaceae), which is commonly referred to as hardy kiwifruit, has been reported to possess anti-inflammatory, anti-allergic and antioxidative properties. The protective effect of the leaves and stems of A. arguta against amyloid β protein (Aβ) (25-35)-induced cultured neuronal cell death and memory impairment was investigated in the current study. Exposure of cultured cortical neurons to 10 μM Aβ (25-35) for 24 h induced significant neuronal death as assessed by a 3-[4,5-dimethylthiazol- 2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. However, A. arguta (10 and 50 μg/ ml) prevented Aβ (25-35)-induced apoptotic neuronal death in cultured cortical neurons. A. arguta also inhibited the 100 μM H2O2-induced decrease of the MTT reduction rate in cultured neurons. Memory impairment was produced by intracerebroventricular microinjection of 15 nmol Aβ (25- 35) and examined using the passive avoidance test in ICR mice. Chronic treatments with A. arguta (50 and 100 mg/ kg, 14 days, p.o.) significantly prevented memory impairment induced by Aβ (25-35), and A. arguta inhibited the Aβ (25-35)-induced increase of cholinesterase activity in the brains of memory impaired mice. These results suggest that A. arguta might be able to inhibit Aβ (25-35)-induced neuronal death and memory impairment via antioxidative and anti-cholinesterase effects and that A. arguta could have a therapeutic role for preventing the progression of neurodegeneration in Alzheimer’s disease.

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