Inflammation after intracerebral hemorrhage

被引:621
作者
Wang, Jian
Dore, Sylvain
机构
[1] Johns Hopkins Univ, Dept Anesthesiol Crit Care Med, Sch Med, Baltimore, MD 21205 USA
[2] Johns Hopkins Univ, Dept Neurosci, Sch Med, Baltimore, MD 21205 USA
关键词
cytokines; hemorrhagic stroke; leukocytes; microglia; reactive oxygen species;
D O I
10.1038/sj.jcbfm.9600403
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Intracerebral hemorrhage ( ICH) is a devastating clinical event without effective therapies. Increasing evidence suggests that inflammatory mechanisms are involved in the progression of ICH-induced brain injury. Inflammation is mediated by cellular components, such as leukocytes and microglia, and molecular components, including prostaglandins, chemokines, cytokines, extracellular proteases, and reactive oxygen species. Better understanding of the role of the ICH-induced inflammatory response and its potential for modulation might have profound implications for patient treatment. In this review, a summary of the available literature on the inflammatory responses after ICH is presented along with discussion of some of the emerging opportunities for potential therapeutic strategies. In the near future, additional strategies that target inflammation could offer exciting new promise in the therapeutic approach to ICH.
引用
收藏
页码:894 / 908
页数:15
相关论文
共 162 条
[1]   Matrix metalloproteinase-9 concentration after spontaneous intracerebral hemorrhage [J].
Abilleira, S ;
Montaner, J ;
Molina, CA ;
Monasterio, J ;
Castillo, J ;
Alvarez-Sabín, J .
JOURNAL OF NEUROSURGERY, 2003, 99 (01) :65-70
[2]   Interleukin-1 and neuronal injury [J].
Allan, SM ;
Tyrrell, PJ ;
Rothwell, NJ .
NATURE REVIEWS IMMUNOLOGY, 2005, 5 (08) :629-640
[3]  
Aloisi F, 1997, J IMMUNOL, V159, P1604
[4]   Temporal profile of matrix metalloproteinases and their inhibitors after spontaneous intracerebral hemorrhage -: Relationship to clinical and radiological outcome [J].
Alvarez-Sabín, J ;
Delgado, P ;
Abilleira, S ;
Molina, CA ;
Arenillas, J ;
Ribó, M ;
Santamarina, E ;
Quintana, M ;
Monasterio, J ;
Montaner, J .
STROKE, 2004, 35 (06) :1316-1322
[5]   Experimental animal models of intracerebral hemorrhage [J].
Andaluz, N ;
Zuccarello, M ;
Wagner, KR .
NEUROSURGERY CLINICS OF NORTH AMERICA, 2002, 13 (03) :385-+
[6]   New horizons for primary intracerebral hemorrhage treatment: experience from preclinical studies [J].
Aronowski, J ;
Hall, CE .
NEUROLOGICAL RESEARCH, 2005, 27 (03) :268-279
[7]   Reduction of tissue plasminogen activator-induced hemorrhage and brain injury by free radical spin trapping after embolic focal cerebral ischemia in rats [J].
Asahi, M ;
Asahi, K ;
Wang, XY ;
Lo, EH .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2000, 20 (03) :452-457
[8]   The radical scavenger edaravone prevents oxidative neurotoxicity induced by peroxynitrite and activated microglia [J].
Banno, M ;
Mizuno, T ;
Kato, H ;
Zhang, GQ ;
Kawanokuchi, J ;
Wang, JY ;
Kuno, R ;
Jin, S ;
Takeuchi, H ;
Suzumura, A .
NEUROPHARMACOLOGY, 2005, 48 (02) :283-290
[9]   Mechanisms of disease - Nuclear factor-kappa b - A pivotal transcription factor in chronic inflammatory diseases [J].
Barnes, PJ ;
Larin, M .
NEW ENGLAND JOURNAL OF MEDICINE, 1997, 336 (15) :1066-1071
[10]   Inflammatory mediators and stroke: New opportunities for novel therapeutics [J].
Barone, FC ;
Feuerstein, GZ .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1999, 19 (08) :819-834