Fustin Flavonoid Attenuates beta-Amyloid (1-42)-Induced Learning Impairment
- Authors
- Jin, CH[Jin, Chun-Hui]; Shin, EJ[Shin, Eun-Joo]; Park, JB[Park, Jae-Bong]; Jang, CG[Jang, Choon-Gon]; Li, ZY[Li, Zhengyi]; Kim, MS[Kim, Min Soo]; Koo, KH[Koo, Kyo Hwan]; Yoon, HJ[Yoon, Hyoung-Jong]; Park, SJ[Park, Sang-Jae]; Choi, WC[Choi, Won-Cheol]; Yamada, K[Yamada, Kiyofumi]; Nabeshima, T[Nabeshima, Toshitaka]; Kim, HC[Kim, Hyoung-Chun]
- Issue Date
- Dec-2009
- Publisher
- WILEY-BLACKWELL
- Citation
- JOURNAL OF NEUROSCIENCE RESEARCH, v.87, no.16, pp.3658 - 3670
- Indexed
- SCIE
SCOPUS
- Journal Title
- JOURNAL OF NEUROSCIENCE RESEARCH
- Volume
- 87
- Number
- 16
- Start Page
- 3658
- End Page
- 3670
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/76399
- DOI
- 10.1002/jnr.22159
- ISSN
- 0360-4012
- Abstract
- Natural flavonoids ameliorate amyloid-beta peptide (A beta)-induced neurotoxicity. We examined whether the fustin flavonoid affects A beta-induced learning impairment in mice. Repeated treatment with fustin significantly attenuated A beta (1-42)-induced conditioned fear and passive avoidance behaviors. This effect was comparable to that of EGb761, a standard extract of ginkgo. Fustin treatment significantly prevented decreases in acetylcholine (ACh) levels, choline acetyltransferase (ChAT) activity, and ChAT gene expression induced by A beta (1-42). Fustin also consistently suppressed increases in acetyl cholinesterase (AChE) activity and AChE gene expression induced by A beta (1-42). In addition, fustin significantly attenuated A beta (1-42)-induced selective decreases in muscarinic M1 receptor gene expression and muscarinic M1 receptor binding activity (as determined by [H-3]pirenzepine binding) by modulating extracellular signal-regulated kinase 1/2 (ERK 1/2) and cAMP response-element binding protein (CREB) phosphorylation and brain-derived neurotrophic factor (BDNF) expression. These effects of fustin were reversed by treatment with dicyclomine, a muscarinic M1 receptor antagonist, and SL327, a selective ERK inhibitor, but not by chelerythrine, a pan-protein kinase C (PKC) inhibitor. Taken together, our results suggest that fustin attenuates A beta (1-42)-impaired learning, and that the ERK/CREB/BDNF pathway is important for the M1 receptor-mediated cognition-enhancing effects of fustin. (C) 2009 Wiley-Liss, Inc.
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Collections - Pharmacy > Department of Pharmacy > 1. Journal Articles
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