Neurological Sciences

, Volume 35, Issue 11, pp 1691–1699

Mild hypothermia alleviates excessive autophagy and mitophagy in a rat model of asphyxial cardiac arrest

Authors

  • Jian Lu
    • Department of Emergency and Critical Care MedicineThe Second Affiliated Hospital of Soochow University
  • Hui-Yin Qian
    • Department of Emergency and Critical Care MedicineThe Second Affiliated Hospital of Soochow University
    • Department of Emergency and Critical Care MedicineThe Second Affiliated Hospital of Soochow University
  • Bao-Chun Zhou
    • Department of Emergency and Critical Care MedicineThe Second Affiliated Hospital of Soochow University
  • Yan Xiao
    • Department of Emergency and Critical Care MedicineThe Second Affiliated Hospital of Soochow University
  • Jin-Ning Mao
    • Department of CardiologyThe Second Affiliated Hospital of Soochow University
  • Guo-Yin An
    • Department of CardiologyThe Second Affiliated Hospital of Soochow University
  • Ming-Zhong Rui
    • Department of HematologyThe Second Affiliated Hospital of Soochow University
  • Tao Wang
    • Department of LaboratoryThe Second Affiliated Hospital of Soochow University
  • Chang-Lai Zhu
    • Electron Microscope RoomThe Affiliated Hospital of Nantong University
Original Article

DOI: 10.1007/s10072-014-1813-6

Cite this article as:
Lu, J., Qian, H., Liu, L. et al. Neurol Sci (2014) 35: 1691. doi:10.1007/s10072-014-1813-6

Abstract

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 °C) was induced following CA for 4 h, and animals were rewarmed at a rate of 0.5 °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.

Keywords

Mild hypothermiaAutophagyMitophagyCardiac arrestIschemic/reperfusion injury

Copyright information

© Springer-Verlag Italia 2014