期刊
FEBS JOURNAL
卷 276, 期 1, 页码 46-57出版社
WILEY
DOI: 10.1111/j.1742-4658.2008.06769.x
关键词
cerebral ischemia; ionic homeostasis; kinase; MnSOD; neuroprotection; nitric oxide; postconditioning; preconditioning; stroke; tolerance
资金
- Ministero Affari Esteri, Direzione Generale per la Promozione e la Cooperazione Culturale Fondi Italia-Cina Legge [401/1990 2007-2008]
- Ricerca Finalizzata [RF-FSL-2006 352059]
Because clinical trials of pharmacological neuroprotective strategies in stroke have been disappointing, attention has turned to the brain's own endogenous strategies for neuroprotection. Two endogenous mechanisms have been characterized so far, namely ischemic preconditioning and ischemic postconditioning. The neuroprotective concept of preconditioning is based on the observation that a brief, noninjurious episode of ischemia is able to protect the brain from a subsequent longer ischemic insult. Recently, a hypothesis has been offered that modified reperfusion subsequent to a prolonged ischemic episode may also confer ischemic neuroprotection, a phenomenon termed postconditioning. Many pathways have been proposed as plausible mechanisms to explain the neuroprotection offered by preconditioning and postconditioning. Unfortunately, so far, none of them has clearly identified the mechanism involved in preconditioning and postconditioning. The present article will review the main mechanisms reported to date to explain the neuroprotective effect of both ischemic preconditioning and postconditioning.
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