期刊
BRAIN BEHAVIOR AND IMMUNITY
卷 22, 期 3, 页码 285-298出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbi.2007.09.011
关键词
arachidonic acid; cyclooxygenase-2; prostaglandins; epoxygenase; Eicosanoids; neuroprotection; brain injuries; neuroinflammation; CYP genes; gene regulation and expression
资金
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS054890] Funding Source: NIH RePORTER
- NINDS NIH HHS [R01 NS054890, R01 NS054890-01A2] Funding Source: Medline
Overexpression of COX2 appears to be both a marker and an effector of neural damage after a variety of acquired brain injuries, and in natural or pathological aging of the brain. COX2 inhibitors may be neuroprotective in the brain by reducing prostanoid and free radical synthesis, or by directing arachidonic acid down alternate metabolic pathways. The arachidonic acid shunting hypothesis proposes that COX2 inhibitors' neuroprotective effects may be mediated by increased formation of potentially beneficial eicosanoids. Under conditions where COX2 activity is inhibited, arachidonic acid accumulates or is converted to eicosanoids via lipoxygenases and cytochrome P450 (CYP) epoxygenases. Several P450 eicosanoids have been demonstrated to have beneficial effects in the brain and/or periphery. We suspect that arachidonic acid shunting may be as important to functional recovery after brain injuries as altered prostanoid formation per se. Thus, COX2 inhibition and arachidonic acid shunting have therapeutic implications beyond the suppression of prostaglandin synthesis and free radical formation. (c) 2007 Elsevier Inc. All rights reserved.
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