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

被引:309
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
  • [1] Abe K, 1998, CELL MOL NEUROBIOL, V18, P709, DOI 10.1023/A:1020230220971
  • [2] Adams HP, 1997, DRUGS, V54, P88
  • [3] Effects of moderate, central fluid percussion traumatic brain injury on nitric oxide synthase activity in rats
    Alagarsamy, S
    DeWitt, DS
    Johnson, KM
    [J]. JOURNAL OF NEUROTRAUMA, 1998, 15 (08) : 627 - 633
  • [4] Increasing plasma neopterin and persistent plasma endothelin during follow-up after acute cerebral ischemia
    Anwaar, I
    Gottsäter, A
    Lindgärde, F
    Mattiasson, I
    [J]. ANGIOLOGY, 1999, 50 (01) : 1 - 8
  • [5] Neuroprotective interaction effects of NMDA and AMPA receptor antagonists in an in vitro model of cerebral ischemia
    Arias, RL
    Tasse, JRP
    Bowlby, MR
    [J]. BRAIN RESEARCH, 1999, 816 (02) : 299 - 308
  • [6] Combined neuroprotection and reperfusion therapy for stroke - Effect of lubeluzole and diaspirin cross-linked hemoglobin in experimental focal ischemia
    Aronowski, J
    Strong, R
    Grotta, JC
    [J]. STROKE, 1996, 27 (09) : 1571 - 1576
  • [7] Neurofilament proteolysis after focal ischemia; When do cells die after experimental stroke?
    Aronowski, J
    Cho, KH
    Strong, R
    Grotta, JC
    [J]. JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1999, 19 (06) : 652 - 660
  • [8] The role of inflammation and cytokines in brain injury
    Arvin, B
    Neville, LF
    Barone, FC
    Feuerstein, GZ
    [J]. NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS, 1996, 20 (03) : 445 - 452
  • [9] Core and penumbral nitric oxide synthase activity during cerebral ischemia and reperfusion
    Ashwal, S
    Tone, B
    Tian, HR
    Cole, DJ
    Pearce, WJ
    [J]. STROKE, 1998, 29 (05) : 1037 - 1046
  • [10] Diffusion- and T-2-weighted MRI of closed-head injury in rats: A time course study and correlation with histology
    Assaf, Y
    BeitYannai, E
    Shohami, E
    Berman, E
    Cohen, Y
    [J]. MAGNETIC RESONANCE IMAGING, 1997, 15 (01) : 77 - 85