Cholinergic anti-inflammatory pathway: a possible approach to protect against myocardial ischemia reperfusion injury / 中华医学杂志(英文版)
Chinese Medical Journal
; (24): 2720-2726, 2010.
Artigo
em Inglês
| WPRIM (Pacífico Ocidental)
| ID: wpr-285758
Biblioteca responsável:
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>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.</p><p><b>DATA SOURCES</b>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".</p><p><b>STUDY SELECTION</b>(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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSIONS</b>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.</p>
Texto completo:
Disponível
Base de dados:
WPRIM (Pacífico Ocidental)
Assunto principal:
Traumatismo por Reperfusão Miocárdica
/
Citocinas
/
Alergia e Imunologia
/
Estimulação do Nervo Vago
/
Inflamação
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Metabolismo
/
Modelos Biológicos
Limite:
Animais
/
Humanos
Idioma:
Inglês
Revista:
Chinese Medical Journal
Ano de publicação:
2010
Tipo de documento:
Artigo