한빛사 논문
Tae Il Kima, Yong Kyung Leea, Sang Gi Parkb, Im Seop Choia, Jung Ok Bana, Hyoung Kook Parkb, Sang-Yoon Namc, Young Won Yunc, Sang Bae Hana, Ki Wan Oha, Jin Tae Honga,*
a College of Pharmacy and CBITRC, Chungbuk National University, Cheongju, Chungbuk 361-763, Korea
b LG Household and Health Care Research Park, Yuseung-Gu, Daejeon 305-343, Korea
c College of Veterinary Medicine and Research Institute of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk 361-763, Korea
*Corresponding author : Jin Tae Hong
Abstract
Amyloid β (Aβ)-induced neurotoxicity is a major pathological mechanism of Alzheimer disease (AD). In this study, we investigated the inhibitory effect of l-theanine, a component of green tea (Camellia sinensis), on Aβ1-42-induced neuronal cell death and memory impairment. Oral treatment of l-theanine (2 and 4 mg/kg) for 5 weeks in the drinking water of mice, followed by injection of Aβ1-42 (2 μg/mouse, icv), significantly attenuated Aβ1-42-induced memory impairment. Furthermore, l-theanine reduced Aβ1-42 levels and the accompanying Aβ1-42-induced neuronal cell death in the cortex and hippocampus of the brain. Moreover, l-theanine inhibited Aβ1-42-induced extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase as well as the activity of nuclear factor κB (NF-κB). l-Theanine also significantly reduced oxidative protein and lipid damage and the elevation of glutathione levels in the brain. These data suggest that the positive effects of l-theanine on memory may be mediated by suppression of ERK/p38 and NF-κB as well as the reduction of macromolecular oxidative damage. Thus, l-theanine may be useful in the prevention and treatment of AD.
Keywords : l-Theanine; Alzheimer disease; Amyloid β; MAP kinases; NF-κB; Oxidative stress; Cell death; Free radicals
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