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Deferoxamine-activated hypoxia-inducible factor-1 restores cardioprotective effects of sevoflurane postconditioning in diabetic rats.

Protección miocárdica - Jue, 03/23/2017 - 00:54
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Deferoxamine-activated hypoxia-inducible factor-1 restores cardioprotective effects of sevoflurane postconditioning in diabetic rats.

Acta Physiol (Oxf). 2017 Mar 17;:

Authors: Xie P, Yang L, Talaiti A, Wu J, Yu J, Yu T, Wang H, Huang B, Wu Q, Maimaitili Y, Wang J, Ma H, Yang Y, Zheng H

Abstract
AIM: The cardioprotective effects of sevoflurane postconditioning (SpostC) are eliminated under diabetic conditions, and the underlying mechanism for this phenomenon remains unclear. Many studies have demonstrated that the hypoxia-inducible factor-1(HIF-1) signaling pathway in the myocardium is impaired under diabetic conditions. This study was to investigate whether deferoxamine (DFO)-induced activation of HIF-1 signaling pathway can restore the cardioprotective effects of SpostC in diabetic rats.
METHODS: A model of myocardial ischemia/reperfusion (I/R) injury was induced via ligation of the left anterior descending artery. SpostC was conducted by administering 1.0 MAC sevoflurane. After inducing the I/R injury, the following parameters were measured: myocardial infarct size, cardiac function, myocardial ultrastructure, mitochondrial respiratory function, respiratory chain enzyme activity, rate of reactive oxygen species (ROS) generation, and protein expression of HIF-1α, vascular endothelial growth factor (VEGF), cleaved caspase-3, Bcl-2 and Bax.
RESULTS: After DFO activated HIF-1 in the impaired myocardium of diabetic rats, SpostC significantly upregulated the protein expression of HIF-1α and its downstream mediator VEGF. This improved myocardial mitochondrial respiratory function and respiratory chain enzyme activity and reduced ROS generation as well as the protein expression of cleaved caspase-3 and Bax. As a result, myocardial infarct size decreased, and cardiac function and mitochondrial ultrastructure improved.
CONCLUSION: This study demonstrates for the first time that abolishment of the cardioprotective effects of SpostC in diabetic rats is associated with impairment of the HIF-1 signaling pathway, and that DFO can activate HIF-1 to restore these cardioprotective effects of SpostC in diabetic rats. This article is protected by copyright. All rights reserved.

PMID: 28316125 [PubMed - as supplied by publisher]

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