The distinct roles of cyclooxygenase-1 and -2 in neuroinflammation: implications for translational research

被引:311
作者
Choi, Sang-Ho [1 ]
Aid, Saba [1 ]
Bosetti, Francesca [1 ]
机构
[1] NIA, Mol Neurosci Unit, Brain Physiol & Metab Sect, NIH, Bethesda, MD 20892 USA
关键词
NONSTEROIDAL ANTIINFLAMMATORY DRUGS; TRAUMATIC BRAIN-INJURY; AMYOTROPHIC-LATERAL-SCLEROSIS; ALZHEIMERS-DISEASE; PARKINSON-DISEASE; PROSTAGLANDIN E-2; MICROGLIAL ACTIVATION; INFLAMMATORY PROCESSES; PHOSPHOLIPASE A(2); CEREBRAL-ISCHEMIA;
D O I
10.1016/j.tips.2009.01.002
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Cyclooxygenases (COX-1 and COX-2) are key enzymes in the conversion of arachidonic acid to prostaglandins and other lipid mediators. Because it can be induced by inflammatory stimuli, COX-2 has been classically considered as the most appropriate target for anti-inflammatory drugs. However, recent data indicate that COX-2 can mediate neuroprotection and that COX-1 is a major player in the neuroinflammatory process. We discuss the specific contributions of COX-1 and COX-2 in various neurodegenerative diseases and in models of neuroinflammation. We suggest that, owing to its predominant localization in microglia, COX-1 might be the major player in neuroinflammation, whereas COX-2, which is localized in neurons, might have a major role in models in which the neurons are directly challenged. Overall, the benefit of using COX-2 inhibitors should be carefully evaluated and COX-1 preferential inhibitors should be further investigated as a potential therapeutic approach in neurodegenerative diseases with an inflammatory component.
引用
收藏
页码:174 / 181
页数:8
相关论文
共 76 条
[1]   Genetic Disruption of Cyclooxygenase-2 Does Not Improve Histological or Behavioral Outcome After Traumatic Brain Injury in Mice [J].
Ahmad, Muzamil ;
Rose, Marie E. ;
Vagni, Vincent ;
Griffith, Raymond P. ;
Dixon, C. Edward ;
Kochanek, Patrick M. ;
Hickey, Robert W. ;
Graham, Steven H. .
JOURNAL OF NEUROSCIENCE RESEARCH, 2008, 86 (16) :3605-3612
[2]   Gene expression of cyclooxygenase-1 and Ca2+-independent phospholipase A2 is altered in rat hippocampus during normal aging [J].
Aid, Saba ;
Bosetti, Francesca .
BRAIN RESEARCH BULLETIN, 2007, 73 (1-3) :108-113
[3]   Neuroinflammatory response to lipopolysaccharide is exacerbated in mice genetically deficient in cyclooxygenase-2 [J].
Aid, Saba ;
Langenbach, Robert ;
Bosetti, Francesca .
JOURNAL OF NEUROINFLAMMATION, 2008, 5 (1)
[4]   Is prostaglandin E2 a pathogenic factor in amyotrophic lateral sclerosis? [J].
Almer, Gabriele ;
Kikuchi, Hitoshi ;
Teismann, Peter ;
Przedborski, Serge .
ANNALS OF NEUROLOGY, 2006, 59 (06) :980-983
[5]   Selective COX-2 inhibitors and dual acting anti-inflammatory drugs: Critical remarks [J].
Bertolini, A ;
Ottani, A ;
Sandrini, M .
CURRENT MEDICINAL CHEMISTRY, 2002, 9 (10) :1033-1043
[6]   Cyclooxygenase 2 (COX-2) inhibition increases the inflammatory response in the brain during systemic immune stimuli [J].
Blais, V ;
Turrin, NP ;
Rivest, S .
JOURNAL OF NEUROCHEMISTRY, 2005, 95 (06) :1563-1574
[7]   Microglia-mediated neurotoxicity: uncovering the molecular mechanisms [J].
Block, Michelle L. ;
Zecca, Luigi ;
Hong, Jau-Shyong .
NATURE REVIEWS NEUROSCIENCE, 2007, 8 (01) :57-69
[8]   Nonsteroidal anti-inflammatory drugs and the risk of Parkinson disease [J].
Bornebroek, Marjolijn ;
de Lau, Lonneke M. L. ;
Haag, Mendel D. M. ;
Koudstaal, Peter J. ;
Hofman, Albert ;
Stricker, Bruno H. C. ;
Breteler, Monique M. B. .
NEUROEPIDEMIOLOGY, 2007, 28 (04) :193-196
[9]   Prostaglandin E2 and microsomal prostaglandin E synthase-2 expression are decreased in the cyclooxygenase-2-deficient mouse brain despite compensatory induction of cyclooxygenase-1 and Ca2+-dependent phospholipase A2 [J].
Bosetti, F ;
Langenbach, R ;
Weerasinghe, GR .
JOURNAL OF NEUROCHEMISTRY, 2004, 91 (06) :1389-1397
[10]   Arachidonic acid metabolism in brain physiology and pathology: lessons from genetically altered mouse models [J].
Bosetti, Francesca .
JOURNAL OF NEUROCHEMISTRY, 2007, 102 (03) :577-586