机构：[1]Department of Emergency and Critical Care Medicine, The Second Affiliated Hospital of Soochow University, Sanxiang Road No. 1055, Suzhou 215000, Jiangsu, People’s Republic of China[2]Department of Cardiology, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, People’s Republic of China[3]Department of Hematology, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, People’s Republic of China[4]Department of Laboratory, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, People’s Republic of China[5]Electron Microscope Room, The Affiliated Hospital of Nantong University, Nantong, Jiangsu, People’s Republic of China
Mild hypothermia is an effective therapeutic strategy to improve poor neurological outcomes in patients following cardiac arrest (CA). However, the underlying mechanism remains unclear. The aim of the study was to evaluate the effect of mild hypothermia on intracellular autophagy and mitophagy in hippocampal neurons in a rat model of CA. CA was induced in Sprague-Dawley (SD) rats by asphyxia for 5 min. After successful resuscitation, the surviving rats were randomly divided into two groups, the normothermia (NT) group and the hypothermia (HT) group. Mild hypothermia (32 A degrees C) was induced following CA for 4 h, and animals were rewarmed at a rate of 0.5 A degrees C/h. Neurologic deficit scores (NDS) were used to determine the status of neurological function. Cytoplasmic and mitochondrial protein from the hippocampus was extracted, and the expression of LC3B-II/I and Parkin were measured as markers of intracellular autophagy and mitophagy, respectively. Of the 60 rats that underwent CA, 44 were successfully resuscitated (73 %), and 33 survived until the end of the experiment (55 %). Mild hypothermia maintained eumorphism of nuclear and mitochondrial structures and significantly improved NDS (p < 0.05). Expression of LC3B-II/I and Parkin in hippocampal nerve cells were significantly increased (p < 0.05) in the NT group relative to the control. Meanwhile, mild hypothermia reduced the level of LC3B-II/I and Parkin (p < 0.05) relative to the NT group. Mild hypothermia protected mitochondria and improved neurological function following CA and resuscitation after ischemia/reperfusion (I/R) injury, likely by reducing excessive autophagy and mitophagy in neurons.
第一作者机构：[1]Department of Emergency and Critical Care Medicine, The Second Affiliated Hospital of Soochow University, Sanxiang Road No. 1055, Suzhou 215000, Jiangsu, People’s Republic of China
通讯作者：
通讯机构：[1]Department of Emergency and Critical Care Medicine, The Second Affiliated Hospital of Soochow University, Sanxiang Road No. 1055, Suzhou 215000, Jiangsu, People’s Republic of China
推荐引用方式(GB/T 7714)：
Jian Lu,Hui-Yin Qian,Li-Jun Liu,et al.Mild hypothermia alleviates excessive autophagy and mitophagy in a rat model of asphyxial cardiac arrest[J].NEUROLOGICAL SCIENCES.2014,35(11):1691-9.doi:10.1007/s10072-014-1813-6.
APA：
Jian Lu,Hui-Yin Qian,Li-Jun Liu,Bao-Chun Zhou,Yan Xiao...&Chang-Lai Zhu.(2014).Mild hypothermia alleviates excessive autophagy and mitophagy in a rat model of asphyxial cardiac arrest.NEUROLOGICAL SCIENCES,35,(11)
MLA：
Jian Lu,et al."Mild hypothermia alleviates excessive autophagy and mitophagy in a rat model of asphyxial cardiac arrest".NEUROLOGICAL SCIENCES 35..11(2014):1691-9
