Cerebral ischemia and trauma - different etiologies yet similar mechanisms: neuroprotective opportunities

被引:310
作者
Leker, RR
Shohami, E
机构
[1] Hadassah Univ Hosp, Dept Neurol, IL-91120 Jerusalem, Israel
[2] Hebrew Univ Jerusalem, Hadassah Med Sch, Dept Neurol, IL-91010 Jerusalem, Israel
[3] Hebrew Univ Jerusalem, Hadassah Med Sch, Agnes Ginges Ctr Human Neurogenet, IL-91010 Jerusalem, Israel
[4] Hebrew Univ Jerusalem, Hadassah Med Sch, Sch Pharmacol, IL-91010 Jerusalem, Israel
关键词
stroke; traumatic brain injury; neuroprotection;
D O I
10.1016/S0165-0173(02)00157-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Cerebral ischemia leads to brain damage caused by pathogenetic mechanisms that are also activated by neurotrauma. These mechanisms include among others excitotoxicity, over production of free radicals, inflammation and apoptosis. Furthermore, cerebral ischemia and trauma both trigger similar auto-protective mechanisms including the production of heat shock proteins, anti-inflammatory cytokines and endogenous antioxidants. Neuroprotective therapy aims at minimizing the activation of toxic pathways and at enhancing the activity of endogenous neuroprotective mechanisms. The similarities in the damage-producing and endogenous auto-protective mechanisms may imply that neuroprotective compounds found to be active against one of these conditions may indeed be also protective in the other. This review summarizes the pathogenetic events of ischemic and traumatic brain injury and reviews the neuroprotective strategies employed thus far in each of these conditions with a special emphasize on their clinical relevance and on future directions in the field of neuronal protection. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:55 / 73
页数:19
相关论文
共 293 条
[81]  
Forsberg-Nilsson K, 1998, J NEUROSCI RES, V53, P521, DOI 10.1002/(SICI)1097-4547(19980901)53:5<521::AID-JNR2>3.0.CO
[82]  
2-B
[83]  
Förstermann U, 1998, FASEB J, V12, P773
[84]   NITRIC-OXIDE SYNTHASE ISOZYMES - CHARACTERIZATION, PURIFICATION, MOLECULAR-CLONING, AND FUNCTIONS [J].
FORSTERMANN, U ;
CLOSS, EI ;
POLLOCK, JS ;
NAKANE, M ;
SCHWARZ, P ;
GATH, I ;
KLEINERT, H .
HYPERTENSION, 1994, 23 (06) :1121-1131
[85]  
FOSTER AC, 1988, J NEUROSCI, V8, P4745
[86]   Temporal profiles and cellular sources of three nitric oxide synthase isoforms in the brain after experimental contusion [J].
Gahm, C ;
Holmin, S ;
Mathiesen, T .
NEUROSURGERY, 2000, 46 (01) :169-177
[87]   Ischemic and excitotoxic brain injury is enhanced in mice lacking the p55 tumor necrosis factor receptor [J].
Gary, DS ;
Bruce-Keller, AJ ;
Kindy, MS ;
Mattson, MP .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1998, 18 (12) :1283-1287
[88]  
GENTLEMAN SM, 1995, ACTA NEUROPATHOL, V89, P537
[89]   Inhibition of caspases prevents cell death of hippocampal CA1 neurons, but not impairment of hippocampal long-term potentiation following global ischemia [J].
Gillardon, F ;
Kiprianova, I ;
Sandkühler, J ;
Hossmann, KA ;
Spranger, M .
NEUROSCIENCE, 1999, 93 (04) :1219-1222
[90]  
Görlach C, 1999, ADV EXP MED BIOL, V471, P91