An alpha-lipoic acid-vitamin E mixture reduces post-embolism lipid peroxidation, cerebral infarction, and neurological deficit in rats

被引:35
作者
Garcia-Estrada, J
Gonzalez-Perez, O
Gonzalez-Castaneda, RE
Martinez-Contreras, A
Luquin, S
de la Mora, PG
Navarro-Ruiz, A
机构
[1] IMSS, CIBO, Div Neurociencias, Guadalajara 44340, Jalisco, Mexico
[2] CUCS, Dept Neurociencias, Guadalajara, Jalisco, Mexico
[3] Hosp Gen Reg 1, IMSS, Colima, Col, Mexico
[4] CUCS, Inst Enfermedades Neurodegenerat, Guadalajara, Jalisco, Mexico
关键词
lipoate; tocopherol; ischemia; antioxidant; thromboembolism; stroke;
D O I
10.1016/S0168-0102(03)00200-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Oxidative stress increases delayed neuronal death in the brain following ischemia. As a consequence, many attempts to reduce the damage resulting from cerebral ischemia under more highly oxidized conditions have focused on treatments aimed at maintaining the redox equilibrium of the local environment. This study demonstrates the synergistic effects of combining treatments with alphalipoic acid (LA) and vitamin E (VE) as an efficient measure to reduce the damage caused by cerebral ischemia. Two oral therapeutic protocols were examined: intensive treatment (100 mg/kg LA and 140 mg/kg VE for 7 days after ischemia) and prophylactic treatment (20 mg/kg LA and 50 mg/kg VE from 30 days before infarction up to the day of sacrifice). The prophylactic treatment reduced serum lipid peroxidation, and diminished brain infarct volume by approximately 50%. Furthermore, prophylactically treated rats showed a reduction in post-ischemia neurological scores. No significant differences were found in the intensively treated group. Our data indicate that pre-ischemia administration of the LA-VE antioxidant mixture reduced the volume of brain damaged and the functional consequences of embolic infarction. These findings suggest that prophylaxis with an LA-VE mixture may be valuable in reducing cerebral damage levels in patients with a high risk of stroke. (C) 2003 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.
引用
收藏
页码:219 / 224
页数:6
相关论文
共 29 条
[1]   Vitamin E kinetics and the function of tocopherol regulatory proteins [J].
Blatt, DH ;
Leonard, SW ;
Traber, MG .
NUTRITION, 2001, 17 (10) :799-805
[2]   POSTTREATMENT WITH EPC-K1, AN INHIBITOR OF LIPID-PEROXIDATION AND OF PHOSPHOLIPASE-A2 ACTIVITY, REDUCES FUNCTIONAL DEFICITS AFTER GLOBAL-ISCHEMIA IN RATS [J].
BLOCK, F ;
KUNKEL, M ;
SONTAG, KH .
BRAIN RESEARCH BULLETIN, 1995, 36 (03) :257-260
[3]  
CAO X, 1995, FREE RADICAL RES, V25, P365
[4]   Role of oxidants in ischemic brain damage [J].
Chan, PH .
STROKE, 1996, 27 (06) :1124-1129
[5]   Reactive oxygen radicals in signaling and damage in the ischemic brain [J].
Chan, PH .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2001, 21 (01) :2-14
[6]   Improved cardiac performance after ischemia in aged rats supplemented with vitamin E and α-lipoic acid [J].
Coombes, JS ;
Powers, SK ;
Hamilton, KL ;
Demirel, HA ;
Shanely, RA ;
Zergeroglu, MA ;
Sen, CK ;
Packer, L ;
Ji, LL .
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 2000, 279 (06) :R2149-R2155
[7]   Pathobiology of ischaemic stroke: an integrated view [J].
Dirnagl, U ;
Iadecola, C ;
Moskowitz, MA .
TRENDS IN NEUROSCIENCES, 1999, 22 (09) :391-397
[8]   NEURONAL NECROSIS AFTER MIDDLE CEREBRAL-ARTERY OCCLUSION IN WISTAR RATS PROGRESSES AT DIFFERENT TIME INTERVALS IN THE CAUDOPUTAMEN AND THE CORTEX [J].
GARCIA, JH ;
LIU, KF ;
HO, KL .
STROKE, 1995, 26 (04) :636-642
[9]   Beneficial effects of α-lipoic acid plus vitamin E on neurological deficit, reactive gliosis and neuronal remodeling in the penumbra of the ischemic rat brain [J].
Gonzalez-Perez, O ;
Gonzalez-Castañeda, RE ;
Huerta, M ;
Luquin, S ;
Gomez-Pinedo, U ;
Sanchez-Almaraz, E ;
Navarro-Ruiz, A ;
Garcia-Estrada, J .
NEUROSCIENCE LETTERS, 2002, 321 (1-2) :100-104
[10]   SUPEROXIDE-DISMUTASE DELAYS NEURONAL APOPTOSIS - A ROLE FOR REACTIVE OXYGEN SPECIES IN PROGRAMMED NEURONAL DEATH [J].
GREENLUND, LJS ;
DECKWERTH, TL ;
JOHNSON, EM .
NEURON, 1995, 14 (02) :303-315