• Biao Xie, XuHui Gao, Yang Huang, Yu Zhang, and Shuibo Zhu.
• Department of Thoracic Cardiovascular Surgery, General Hospital of Central Theater Command, Wuhan, China.
• Shock. 2021 Jan 1; 55 (1): 74-82.

BackgroundStudies have shown that remote ischemic post-conditioning can improve brain damage caused by ischemia and hypoxia. However, the specific mechanism underlying this phenomenon is still unclear. The purpose of this study was to investigate the effects of remote ischemic post-conditioning on neuronal apoptosis and mitophagy after cardiopulmonary resuscitation (CPR) in rats.MethodsMale Sprague-Dawley rats were used to establish an asphyxia cardiac arrest model by clamping the tracheal duct. First, the expression levels of P53, Cytochrome c (Cytc), and Parkin in the cytoplasm and mitochondria were observed at 3, 6, 24, and 72 h after the restoration of spontaneous circulation (ROSC). Then neurological deficit scores, hippocampal neuron apoptosis, mitochondrial P53 and Parkin, cytoplasmic Cytc, and neuron ultrastructure were evaluated 24 h after ROSC.ResultsP53 and Parkin can translocate from the cytoplasm to the mitochondria, promoting the translocation of cytoplasmic Cytc to mitochondria after CPR, reaching a peak at 24 h after the ROSC. The P53 inhibitor Pifithrin-μ reduced apoptosis induced by P53 mitochondrial translocation. Apoptosis was induced after cardiac arrest and attenuated by remote ischemic postconditioning via inhibiting P53 mitochondrial translocation and the release of Cytc to the cytoplasm. In addition, remote ischemic postconditioning could inhibit Parkin-mediated mitophagy.ConclusionTaken together, our results show that remote ischemic post-conditioning improves neural function after CPR by inhibiting P53 mitochondrial translocation-induced apoptosis and Parkin-mediated mitophagy.Copyright © 2020 by the Shock Society.

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