Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 436, Issue 2, Pages 180-185Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2013.05.070
Keywords
Ischemia/reperfusion; NF-kappa B; Autophagy
Categories
Funding
- Natural Science Foundation of China [81260043, 81100153]
- Natural Science Foundation of Hainan province [310130]
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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.
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