Sulforaphane improves cognitive function administered following traumatic brain injury

被引:115
作者
Dash, Prarnod K. [1 ]
Zhao, Jing [1 ]
Orsi, Sara A. [1 ]
Zhang, Min [1 ]
Moore, Anthony N. [1 ]
机构
[1] Univ Texas Med Sch, Dept Neurobiol & Anat, Houston, TX 77225 USA
基金
美国国家卫生研究院;
关键词
TBI; Nrf2; Prefrontal cortex; Hippocampus; Spatial memory; CONTROLLED CORTICAL IMPACT; OLIGONUCLEOTIDE MICROARRAY; MEMORY DEFICITS; EXPRESSION; IDENTIFICATION; NEURONS; COMPLEX; PROTEIN; STRESS; MODEL;
D O I
10.1016/j.neulet.2009.04.028
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Recent studies have shown that sulforaphane, a naturally occurring compound that is found in cruciferous vegetables, offers cellular protection in several models of brain injury. When administered following traumatic brain injury (TBI), sulforaphane has been demonstrated to attenuate blood-brain barrier permeability and reduce cerebral edema. These beneficial effects of sulforaphane have been shown to involve induction of a group of cytoprotective, Nrf2-driven genes, whose protein products include free radical scavenging and detoxifying enzymes. However, the influence of sulforaphane on post-injury cognitive deficits has not been examined. In this study, we examined if sulforaphane, when administered following cortical impact injury, can improve the performance of rats tested in hippocampal- and prefrontal cortex-dependent tasks. Our results indicate that sulforaphane treatment improves performance in the Morris water maze task (as indicated by decreased latencies during learning and platform localization during a probe trial) and reduces working memory dysfunction (tested using the delayed match-to-place task). These behavioral improvements were only observed when the treatment was initiated 1 h, but not 6 h, post-injury. These studies support the use of sulforaphane in the treatment of TBI, and extend the previously observed protective effects to include enhanced cognition. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:103 / 107
页数:5
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