Crucial role of endogenous interleukin-10 production in myocardial ischemia/reperfusion injury

Article

关键词: NITRIC-OXIDE SYNTHASE;    INTERCELLULAR-ADHESION MOLECULE-1;    TUMOR-NECROSIS-FACTOR;    ISCHEMIA-REPERFUSION;    CONSCIOUS RABBITS;    INTERFERON-GAMMA;    P-SELECTIN;    MICE;    IL-10;    INFARCTION;   

DOI  :  10.1161/01.CIR.101.9.1019

来源: SCIE

【 摘 要 】

Background-The anti-inflammatory cytokine interleukin-10 (IL-10) has been detected in the plasma of patients with myocardial ischemia/reperfusion. The aim of our study was to investigate the role of endogenously produced IL-10 in myocardial ischemia/reperfusion. Methods and Results-In the present study, we used wild-type and IL-10-deficient mice subjected to myocardial ischemia/reperfusion. Significant levels of IL-10 were produced in wild-type mice at 2 to 6 hours after myocardial reperfusion, The genetic deletion of IL-10 enhanced neutrophil infiltration into the reperfused tissues at 6 hours after reperfusion and increased infarct size and myocardial necrosis. Furthermore, in the absence of IL-10, an enhancement of the inflammatory response was seen, as demonstrated by increased plasma levels of tumor necrosis factor-alpha, nitrite/nitrate (breakdown products of NO), and increased tissue expression of intercellular adhesion molecule-1. Reperfusion for 24 hours was associated with a 75% mortality rate in IL-10- deficient mice, whereas no deaths occurred in the wild-type animals. Conclusions-The present findings provide the first direct evidence that endogenous IL-10 inhibits the production of tumor necrosis factor-ct and NO and serves to protect the isehemic and reperfused myocardium through the suppression of neutrophil recruitment.

【 授权许可】

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