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자료유형
학술저널
저자정보
Jo, Mi-Ran (College of Pharmacy and Medical Research Center, Chungbuk National University) Park, Mi-Hee (College of Pharmacy and Medical Research Center, Chungbuk National University) Choi, Dong-Young (College of Pharmacy and Medical Research Center, Chungbuk National University) Yuk, Dong-Yeun (College of Pharmacy and Medical Research Center, Chungbuk National University) Lee, Yuk-Mo (College of Pharmacy and Medical Research Center, Chungbuk National University) Lee, Jin-Moo (College of Pharmacy and Medical Research Center, Chungbuk National University) Jeong, Jae-Hwang (Department of Biotechnology and Bioinformatics, Chungbuk Provincial College of Science & Technology) Oh, Ki-Wan (College of Pharmacy and Medical Research Center, Chungbuk National University) Lee, Moon-Soon (College of Chungbuk National University) Han, Sang-Bae (College of Pharmacy and Medical Research Center, Chungbuk National University) Hong, Jin-Tae (College of Pharmacy and Medical Research Center, Chungbuk National University)
저널정보
한국응용약물학회 Biomolecules & Therapeutics(구 응용약물학회지) Biomolecules & therapeutics 제19권 제3호
발행연도
2011.1
수록면
288 - 295 (8page)

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Amyloid beta ($A{\beta}$)-induced neurotoxicity is a major pathological mechanism of Alzheimer's disease (AD). In this study, we investigated the inhibitory effect of L-theanine, a component of green tea (Camellia sinensis) on $A{\beta}_{1-42}$-induced neurotoxicity and oxidative damages of macromolecules. L-theanine inhibited $A{\beta}_{1-42}$-induced generation of reactive oxygen species, and activation of extracellular signal-regulated kinase and p38 mitogenic activated protein kinase as well as the activity of nuclear factor kappa-B. L-theanine also signifi cantly reduced oxidative protein and lipid damage, and elevated glutathione level. Consistent with the reduced neurotoxic signals, L-theanine (10-50 ${\mu}g$/ml) concomitantly attenuated $A{\beta}_{1-42}$ (5 ${\mu}M$)-induced neurotoxicity in SK-N-MC and SK-N-SH human neuroblastoma cells. These data indicate that L-theanine on $A{\beta}$-induced neurotoxicity prevented oxidative damages of neuronal cells, and may be useful in the prevention and treatment of neurodegenerative disease like AD.

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