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Cholinergic anti-inflammatory pathway: a possible approach to protect against myocardial ischemia reperfusion injury 被引量:33
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作者 XIONG Jun XUE Fu-shan YUAN Yu-jing WANG Qiang LIAO Xu WANG Wei-li 《Chinese Medical Journal》 SCIE CAS CSCD 2010年第19期2720-2726,共7页
Objective A general review was made of studies involving: (1) the concept and mechanism of the cholinergic anti-inflammatory pathway (CAP), (2) the important role of inflammatory response in myocardial ischemia... Objective A general review was made of studies involving: (1) the concept and mechanism of the cholinergic anti-inflammatory pathway (CAP), (2) the important role of inflammatory response in myocardial ischemia reperfusion (I/R) injury and (3) the evidence and mechanisms by which CAP may provide protection against myocardial I/R injury. Data sources The data used in this review were mainly from manuscripts listed in PubMed that were published in English from 1987 to 2009. The search terms were "vagal nerve stimulation", "myocardial ischemia reperfusion injury", "nicotine acetylcholine receptor" and "inflammation". Study selection (1) Clinical and experimental evidence that the inflammatory response induced by reperfusion enhances myocardial I/R injury. (2) Clinical and laboratory evidence that the CAP inhibits the inflammation and provides protection against myocardial I/R injury. Results The myocardial I/R injury is really an inflammatory process characterized by recruitment of neutrophils into the ischemic myocardium and excessive production of pro-inflammatory cytokines. Because the CAP can modulate the inflammatory response by decreasing the production and release of pro-inflammatory cytokines, it can provide protection against myocardial I/R injury. Conclusions The CAP can inhibit the inflammatory response induced by reperfusion and protect against myocardial I/R injury. It represents an exciting opportunity to develop new and novel therapeutics to attenuate the myocardial I/R injury. 展开更多
关键词 vagal nerve stimulation myocardial ischemia reperfusion injury nicotine acetylcholine receptor CYTOKINES INFLAMMATION
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