Administration of riboflavin improves behavioral outcome and reduces edema formation and glial fibrillary acidic protein expression after traumatic brain injury

被引:46
作者
Hoane, MR [1 ]
Wolyniak, JG [1 ]
Akstulewicz, SL [1 ]
机构
[1] So Illinois Univ, Dept Psychol, Restorat Neurosci Lab, Brain & Cognit Sci Program, Carbondale, IL 62901 USA
关键词
vitamin B-2; Recovery of Function; GFAP; Rat; sensorimotor behavior; antioxidant;
D O I
10.1089/neu.2005.22.1112
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Previous studies have shown that administration of riboflavin, vitamin B-2, significantly reduced edema formation following experimental stroke. The present study evaluated the ability of B-2 to improve behavioral function, reduce edema formation, and limit glial fibrillary acidic protein (GFAP) expression following frontal cortex contusion injury. Groups of rats were assigned to B-2 (7.5 mg/kg) or saline (1.0 ml/kg) treatment conditions and received contusion injuries or sham procedures. Drug treatment was administered 15 min and 24 h following injury. Rats were examined on a variety of tests to measure sensorimotor performance (bilateral tactile removal test), and cognitive ability (acquisition of reference and working memory) in the Morris water maze. Administration of B-2 following injury significantly reduced the behavioral impairments observed on the bilateral tactile removal test and improved the acquisition of both reference and working memory tests compared to saline-treated rats. The lesion analysis showed that B-2 reduced the size of the lesion. Examination of GFAP expression around the lesion revealed that B-2 significantly reduced the number of GFAP(+) astrocytes. Edema formation following injury was also significantly reduced by B-2 administration. These findings are the first to show that B-2 administration significantly improved behavioral outcome and reduced lesion volume, edema formation, and the expression of GFAP following traumatic brain injury. These findings suggest that B-2 may have therapeutic potential for the treatment of TBI.
引用
收藏
页码:1112 / 1122
页数:11
相关论文
共 44 条
[1]   Glutamate neurotoxicity, oxidative stress and mitochondria [J].
Atlante, A ;
Calissano, P ;
Bobba, A ;
Giannattasio, S ;
Marra, E ;
Passarella, S .
FEBS LETTERS, 2001, 497 (01) :1-5
[2]   Nicotinamide reduces infarction up to two hours after the onset of permanent focal cerebral ischemia in Wistar rats [J].
Ayoub, IA ;
Lee, EJ ;
Ogilvy, CS ;
Beal, MF ;
Maynard, KI .
NEUROSCIENCE LETTERS, 1999, 259 (01) :21-24
[3]   Therapeutic window for nicotinamide following transient focal cerebral ischemia [J].
Ayoub, IA ;
Maynard, KI .
NEUROREPORT, 2002, 13 (02) :213-216
[4]   Postinjury treatment with magnesium chloride attenuates cortical damage after traumatic brain injury in rats [J].
Bareyre, FM ;
Saatman, KE ;
Raghupathi, R ;
McIntosh, TK .
JOURNAL OF NEUROTRAUMA, 2000, 17 (11) :1029-1039
[5]  
BETZ AL, 1994, ACTA NEUROCHIR, P314
[6]  
CHRISTENSEN HN, 1993, NUTR REV, V51, P149
[7]   A CONSIDERATION OF NEURAL COUNTING METHODS [J].
COGGESHALL, RE .
TRENDS IN NEUROSCIENCES, 1992, 15 (01) :9-13
[8]   Mitochondrial participation in ischemic and traumatic neural cell death [J].
Fiskum, G .
JOURNAL OF NEUROTRAUMA, 2000, 17 (10) :843-855
[9]   Magnesium attenuates post-traumatic depression/anxiety following diffuse traumatic brain injury in rats [J].
Fromm, L ;
Heath, DL ;
Vink, R ;
Nimmo, AJ .
JOURNAL OF THE AMERICAN COLLEGE OF NUTRITION, 2004, 23 (05) :529S-533S
[10]  
HALL ED, 1993, RES P ARNMD, V71, P81