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Aβ (25-35)에 의해 유도된 신경세포 독성과 기억력 손상에 대한 다래나무 추출물의 보호효과
Protective Effect of Actinidia arguta on Aβ (25-35)-Induced Neuronal Toxicity and Memory Impairment
Background : Alzheimer`s disease (AD) is characterized by neuronal loss and extracellular senile plaque, whose major constituent is β-amyloid (Aβ), a 39-43 amino acid peptide derived from amyloid precursor protein. In cultures, Aβ directly induce neuronal cell death and can include excessive generation of free radicals and peroxidative injury to proteins, lipids, and other macromolecules. Actinidia arguta, generally called hardy kiwifruit, has been reported to possess anti-inflammatory, anti-allergic and antioxidative properties. The present study aims to investigate the neuroprotective effect of the leaves and stems of A. arguta using in vitro cultured neurons and in vivo experimental animals. Methods and Results : Primary cortical neuronal cultures were prepared using Sprague-Dawley (SD) rat fetuses on embryonic days 15. Neurotoxicity experiments were performed on neurons after 3-4 days in culture. Cultured neurons were treated with 10 μM Aβ (25-35) for 24 h to produce neurotoxicity. In addition, cultured neurons were treated with H2O2 (100 μM) for 15 min and then incubated for 12 h in H2O2-free medium. Viability of cultured neurons was measured by a colorimetric MTT assay. Hoechst 33342 staining of neurons was carried out to examine Aβ (25-35)-induced apoptotic neuronal death. A. arguta over the concentration of 10 to 50 ㎍/㎖ prevented Aβ (25-35) (10 μM)-induced apoptotic neuronal death, and inhibited H2O2-induced decrease of MTT reduction rate. These results suggest that oxidative stress is implicated in Aβ (25-35)-induced neuronal apoptotic death. Memory impairment was produced by intracerebroventricular (i.c.v) microinjection of 15 nmol Aß (25-35) and examined using passive avoidance test in ICR mice. Chronic treatments with A. arguta (14 days, p.o.) protected memory impairment induced by Aß (25-35). Conclusion : The present study suggests that A. arguta has a therapeutic role for preventing the progression of neurodegenerative disease such as AD.
