J Biomed Transl Res.  2018 Jun;19(2):26-31. 10.12729/jbtr.2018.19.2.026.

Inhibitory effect of the leaves and stems of Actinidia arguta on Aβ (25–35)-induced neuronal cell death and memory impairment

• Kang SG
• Seong YH

• KMID: 2435752
• DOI: http://doi.org/10.12729/jbtr.2018.19.2.026

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-dimethylthiazol2-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.

Keyword

Actinidia arguta; amyloid β protein; neuroprotection; cultured neurons; memory impairment

MeSH Terms

Actinidia*
Alzheimer Disease
Amyloid
Animals
Brain
Cell Death*
Cholinesterases
Memory*
Mice
Mice, Inbred ICR
Microinjections
Neurons*
Neuroprotection
Amyloid
Cholinesterases