Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 473, Issue 4, Pages 1119-1124Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2016.04.026
Keywords
Pramipexole; Myocardial ischemia/reperfusion injury; Autophagy
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Funding
- Scientific and Technological Research Project of the Education Department in Hunan Province in China [14C1129]
- Chinese medicine research project in Hunan Province in China [201561]
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This article investigated the effects of pramipexole on myocardial ischemia reperfusion (I/R) injury and its underlying mechanisms. We utilized an in vivo mouse model of myocardial I/R injury and an in vitro H9c2 cell model of hypoxia/reoxygenation (H/R) injury. Pramipexole pretreatment in male C57BL/6 mice significantly reduced the myocardial infarction size, decreased the CK and LDH activities at the serum level and enhanced autophagy. In the in vitro study, the pramipexole treatment significantly elevated the survival rate, decreased the LDH activity, reduced ROS generation and restored the Delta Psi m in H9C2 cells during H/R. Additionally, its use could increase the autophagy flux level in H9c2 cells. The underlying mechanisms were determined by measuring the expression of the autophagic protein levels. These results further indicated that pramipexole treatment modulated H/R-induced autophagy via an AMPK-dependent pathway. All of these data indicate that pramipexole exerted protective effects against myocardial I/R injury and enhanced autophagy in part through the AMPK-mediated pathway. (C) 2016 Elsevier Inc. All rights reserved.
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