Amyrin Attenuates Scopolamine-Induced Cognitive Impairment in Mice
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- Park Se Jin
- Department of Life and Nanopharmaceutical Science, Kyung Hee University
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- Ahn Young Je
- Department of Life and Nanopharmaceutical Science, Kyung Hee University
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- Oh Sa Rang
- College of Pharmacy, Keimyung University
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- Lee Younghwan
- Department of Life and Nanopharmaceutical Science, Kyung Hee University
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- Kwon Guyoung
- Department of Life and Nanopharmaceutical Science, Kyung Hee University
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- Woo Hyun
- Department of Life and Nanopharmaceutical Science, Kyung Hee University
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- Lee Hyung Eun
- Department of Life and Nanopharmaceutical Science, Kyung Hee University
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- Jang Dae Sik
- Department of Life and Nanopharmaceutical Science, Kyung Hee University Department of Pharmaceutical Science, College of Pharmacy, Kyung Hee University
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- Jung Ji Wook
- Department of Herbal Medicinal Pharmacology, College of Herbal Bio-industry, Daegu Haany University
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- Ryu Jong Hoon
- Department of Life and Nanopharmaceutical Science, Kyung Hee University Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University
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抄録
Alzheimer’s disease, a neurodegenerative disorder, is characterized by progressive cognitive impairment associated with the disruption of cholinergic neurotransmission. The aim of the present study was to evaluate the effect of α- or β-amyrin, a type of pentacyclic triterpene, on the cognitive impairment induced by scopolamine, a muscarinic acetylcholine receptor antagonist. To measure the abilities of various types of learning and memory, we conducted step-through passive avoidance task. Scopolamine induced deficits in learning and memory processes in mice, which were antagonized by a single administration of α-amyrin (2 or 4 mg/kg) or β-amyrin (4 mg/kg), respectively. Additionally, in vitro analysis revealed that acetylcholinesterase activity was inhibited by β-amyrin, but not by α-amyrin. Furthermore, Western blot analysis revealed that the expression levels of phosphorylated extracellular signal-regulated kinase 1/2 (pERK) and phosphorylated glycogen synthase kinase-3β (pGSK-3β) were significantly enhanced by a single administration of α- and β-amyrin in the hippocampus. Finally, the memory ameliorating effects of α- or β-amyrin on the scopolamine-induced cognitive impairments were significantly blocked by ERK inhibitor U0126. The present study suggests that α- and β-amyrin may ameliorate the cognitive impairment induced by hypocholinergic neurotransmission via the activation of ERK as well as GSK-3β signaling.
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 37 (7), 1207-1213, 2014
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390282679611101184
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- NII論文ID
- 130004057428
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- NII書誌ID
- AA10885497
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- COI
- 1:STN:280:DC%2BC2cfovVGjtg%3D%3D
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 025543327
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- PubMed
- 24989012
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可