The memory ameliorating effects of INM-176, an ethanolic extract of Angelica gigas, against scopolamine- or Aβ1-42-induced cognitive dysfunction in mice

被引:56
|
作者
Park, Se Jin [2 ]
Jung, Jun Man [2 ,3 ]
Lee, Hyung Eun [2 ,3 ]
Lee, Young Woo [2 ,3 ]
Kim, Dong Hyun [2 ,3 ]
Kim, Jong Min [2 ,3 ]
Hong, Jin Gyu [2 ,3 ]
Lee, Chang Hwan [2 ,3 ]
Jung, In Ho [4 ]
Cho, Yong-Baik [4 ]
Jang, Dae Sik [2 ,3 ]
Ryu, Jong Hoon [1 ,2 ,3 ]
机构
[1] Kyung Hee Univ, Dept Oriental Pharmaceut Sci, Coll Pharm, Seoul 130701, South Korea
[2] Dept Life & Nanopharmaceut Sci, Seoul, South Korea
[3] Kyung Hee Univ, Coll Pharm, Kyung Hee EW Pharmaceut Res Inst, Seoul 130701, South Korea
[4] WhanIn Pharmaceut Co Ltd, Seoul 138200, South Korea
关键词
INM-176; Angelica gigas; Neuroprotection; Memory; Amyloid beta protein; Acetylcholinesterase; ALZHEIMERS-DISEASE; IMPAIRMENT; ACETYLCHOLINESTERASE; HYPOTHESIS; PROTECTION; COMPOUND; DECURSIN; AMNESIA; ESP-102;
D O I
10.1016/j.jep.2012.07.019
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Ethnopharmacological relevance: Alzheimer's disease is a neurodegenerative disorder associated with cognitive impairment and cholinergic neuronal death. INM-176 is a standardized ethanolic extract of Angelica gigas Nakai that has been traditionally used in herbal medicine in China, Japan, and Korea to treat anemia or as a sedative. We investigated whether INM-176 exhibits anti-amnesic effects. Materials and methods: Memory impairment was induced by scopolamine, a cholinergic muscarinic receptor antagonist, or amyloid beta(1-42) (A beta(1-42)) protein. Anti-amnesic effects of INM-176 were measured by the passive avoidance and the Morris water maze tasks in mice. We also examined the effect of INM-176 on the acetylcholinesterase activity, as well as A beta(1-42) protein-induced astrogliosis or cholinergic neuronal loss in the brain. Results: Scopolamine-induced cognitive dysfunction was significantly attenuated by a single or sub-chronic administration of INM-176 in the passive avoidance and the Morris water maze tasks. A single or sub-chronic administration of INM-176 also ameliorated memory impairments induced by A beta(1-42) protein. INM-176 inhibited acetylcholinesterase activity in the hippocampal tissue in vitro and ex vivo. In addition, INM-176 attenuated the A beta(1-42) protein-induced astrocyte activation in the hippocampus as well as cholinergic neuronal damage in the CA3 region of the hippocampus and the nucleus basalis of Meynert. Conclusion: These results suggest that the memory ameliorating effects of INM-176 on scopolamine- or A beta(1-42) protein-induced memory impairment are mediated, in part, via acetylcholinesterase inhibition and neuroprotective activities. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:611 / 620
页数:10
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