Changes of neuronal apoptosis and expression of endoplasmic reticulum stress related factors GRP78 and CHOP in rats after cardiopulmonary resuscitation

doi:10.3969/j.issn.1009-6574.2017.10.004

Abstract：Objective To investigate the dynamic changes of endoplasmic reticulum stress-related factors, the expression of glucose regulated protein 78 (GRP78) and CCAAT/ enhancer binding protein homologue protein (CHOP) in rats after cardiac arrest and resuscitation, their relationship with neuronal apoptosis, so as to explore the mechanism of endoplasmic reticulum stress and cerebral ischemia-reperfusion injury. Methods A total of 48 male SD rats were randomly divided into two groups: the group of without cardiopulmonary resuscitation (CPR) (control group) (n=24) and the group of normothermia after CPR (CPR group) (n=24). The CPR model in rats were prepared by esophagus pacing induced ventricular fibrillation. At the time of 6 h, 12 h, 24 h, and 48 h after restoration of spontaneous circulation, the morphology of the surviving neurons in the hippocampal CA1 region of rats was observed by Nissl staining. TUNEL staining was used to observe the apoptosis of hippocampal CA1 neurons in rats and to count the number of positive apoptotic cells. The expression of antigen of GRP78 and CHOP was detected by immunohistochemical method. The expression of GRP78 and CHOP was detected by Western Blot method. Results Compared with control group, the neuronal cell degeneration in the hippocampal CA1 area was more severe in the resuscitation group. Apoptotic cells increased significantly with the increase of reperfusion time. Compared with control group, GRP78 positive cells in the resuscitation group increased gradually at reperfusion 6 h, and increased significantly in 12 h, and then the expression decreased gradually. In the CPR group, CHOP positive cells began to be expressed at the beginning of the reperfusion 6 h, and gradually increased, and increased significantly at 24 h until 48 h. Conclusions Endoplasmic reticulum stress is induced after CA/CPR. It can protect itself at the early stage by upregulated the expression of GRP78 protein, and apoptosis is induced by upregulated apoptosis factor CHOP at the late stage.