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.