NF-κB-mediated induction of autophagy in cardiac ischemia/reperfusion injury

被引:111
|
作者
Zeng, Min [1 ]
Wei, Xin [1 ]
Wu, Zhiyong [1 ]
Li, Wei [1 ]
Li, Bing [1 ]
Zhen, Ying [1 ]
Chen, Jixiong [1 ]
Wang, Ping [1 ]
Fei, Yi [1 ]
机构
[1] Peoples Hosp Hainan Prov, Haikou 570311, Peoples R China
关键词
Ischemia/reperfusion; NF-kappa B; Autophagy; ISCHAEMIA/REPERFUSION INJURY; CELL-DEATH; HEART; REPERFUSION; INHIBITION; ACTIVATION; BECLIN-1;
D O I
10.1016/j.bbrc.2013.05.070
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Ischemia/reperfusion (I/R) injury severely attenuates the benefit of revascularization after acute myocardial infarction, in which transcription factor NF-kappa B plays an important role. Recently, there is increasing evidence to suggest that autophagy is involved in this process. We sought to define the role of NF-kappa B in the induction of autophagy during cardiac I/R injury. The left circumflex coronary arteries of New Zealand white rabbits were ligated for 1.5 h, followed by reperfusion for I h to induce I/R injury. Production of reactive oxygen species (ROS) was detected in myocardial injury area following I/R injury. Furthermore, the results indicated that the cardiac area at risk (AAR) for ischemia has the most abundant expression of Beclin 1 in parallel to p65 expression after cardiac I/R injury. Inhibition of NF-kappa B significantly attenuated Beclin 1 expression and autophagy in the AAR, which was associated with a marked reduction in the extent of the AAR. Our data thus suggests that I/R injury promotes NF-kappa B activity, in response to ROS, to aggravate myocardial injury through the activation of Beclin 1-mediated autophagy. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:180 / 185
页数:6
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