The neuroprotective effects of the seeds of Cassia obtusifolia on transient cerebral global ischemia in mice

被引:71
作者
Kim, Dong Hyun [2 ,3 ]
Kim, Sunho [2 ,3 ]
Jung, Won Yong [2 ,3 ]
Park, Se Jin [2 ,3 ]
Park, Dong Hyun [2 ,3 ]
Kim, Jong Min [2 ,3 ]
Cheong, Jae Hoon [4 ]
Ryu, Jong Hoon [1 ,2 ,3 ]
机构
[1] Kyung Hee Univ, Dept Oriental Pharmaceut Sci, Coll Pharm, Seoul 130701, South Korea
[2] Kyung Hee Univ, Dept Life & Nanopharmaceut Sci, Seoul 130701, South Korea
[3] Kyung Hee Univ, Kyung Hee EW Pharmaceut Res Inst, Coll Pharm, Seoul 130701, South Korea
[4] Sahmyook Univ, Dept Pharm, Seoul 139742, South Korea
关键词
Global ischemia; Glia; iNOS; COX-2; BDNF; pCREB; DELAYED NEURONAL DEATH; NITRIC-OXIDE SYNTHASE; ELEMENT-BINDING PROTEIN; CYCLOOXYGENASE-2; MESSENGER-RNA; NERVE GROWTH-FACTOR; FOREBRAIN ISCHEMIA; HIPPOCAMPAL-NEURONS; GERBIL HIPPOCAMPUS; BRAIN-DAMAGE; GENE-EXPRESSION;
D O I
10.1016/j.fct.2009.03.028
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
The aim of this study was to determine the mechanism underlying the neuroprotective effects of the ethanolic extract of the seeds of Cassia obtusifolia (COE) (10 or 50 mg/kg/day, p.o) on transient cerebral global ischemia induced by bilateral common carotid artery occlusion (2VO) in mice. Immunohistochernical and western blot studies showed that levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in the hippocampal CA1 region at 1 day post-2VO were attenuated by COE (50 mg/kg/day, p.o), which was administered immediately after 2VO. Furthermore, OX-42 - and glial fibrillary acidic protein (GFAP)-positive cell numbers at 4 days post-2VO were markedly attenuated by COE (50 mg/kg/day, p.o) treatment for 4 days in CA1. Viable neurons detected by Nissl at 7 days post-2VO were increased by administering COE (50 mg/kg/day, p.o) for 7 days. In addition, COE increased the expressions of phosphorylated cAMP response element binding protein (CREB) and brain-derived neurotrophic factor (BDNF) in CA1 in naive-control within I and 6 h, respectively, and these expressions were also profoundly increased in 2VO-treated mice by COE at immediately post-2VO. These results suggest that the neuroprotective effects of COE are due to its anti-inflammatory effects and to its upregulation of BDNF expression and CREB phosphorylation. Crown Copyright (C) 2009 Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:1473 / 1479
页数:7
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