CC chemokine receptor-2 deficiency attenuates oxidative stress and infarct size caused by myocardial ischemia-reperfusion in mice
CC chemokine receptor-2 deficiency attenuates oxidative stress and infarct size caused by myocardial ischemia-reperfusion in mice
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DOI：
10.1253/circj.70.342
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发表时间：
2006-03-01
影响因子：
3.3
通讯作者：
Takeya, M
中科院分区：
文献类型：
--
作者：
Hayasaki, T;Kaikita, K;Takeya, M
研究背景单核细胞趋化蛋白-1（MCP-1）及其主要受体CC趋化因子受体2（CCR 2）参与心肌梗死后左室重构。然而，CCR 2缺陷是否对心肌缺血-再灌注后的心肌有保护作用尚不清楚。本研究的目的是探讨CCR 2缺陷对小鼠心肌缺血再灌注损伤的影响。方法和结果实验在CCR 2（-/-）和野生型小鼠进行45分钟的缺血再灌注。与野生型小鼠相比，CCR 2（-/-）小鼠缺血性病变中的巨噬细胞浸润显著减少（p
Background Monocyte chemoattractant protein-1 (MCP-1) and its major receptor, CC chemokine receptor 2 (CCR2), have been shown to contribute to left ventricular remodeling after myocardial infarction. However, it is unknown whether CCR2 deficiency protects the myocardium after myocardial ischemia-reperfusion. The purpose of the present study was to investigate the effects of CCR2 deficiency on myocardial ischemia-reperfusion injury in mice.Methods and Results Experiments were performed in CCR2(-/-) and wild-type mice subjected to 45 min of ischemia followed by reperfusion. Macrophage infiltration in ischemic lesions was markedly reduced in CCR2(-/-) mice compared with wild-type mice (p