Effect of propofol post-conditioning on oxygen-glucose deprivation and restoration-induced abnormal cell cycle activation in hippocampal neurons of rats

Objective To investigate the effect of propofol post-conditioning on oxygen-glucose deprivation and restoration (OGD/R)-induced abnormal cell cycle activation in hippocampal neurons of rats. Methods Primarily cultured hippocampal neurons obtained from fetal Wistar rats were cultured for 7 days and seeded in culture wells (100 μl/well) or in culture flasks (3 ml/flask) at a density of 5×105 cells/ml.The neurons were divided into 3 groups (n=24 each) using a random number table: control group (group C); group OGD/R; propofol post-conditioning group (group PP). The neurons were subjected to oxygen-glucose deprivation for 1 h followed by restoration of oxygen-gulcose supply for 24 h. Propofol 1.2 μg/ml was added immediately after onset of oxygen-glucose restoration, and the neurons were incubated for 2 h in group PP.At 24 h of oxygen-glucose restoration, cells were collected for measurement of the cell viability by methyl thiazolyl tetrazolium assay, and the mitochondrial membrane potential (MMP), intracellular Ca2+ concentration ([Ca2+ ]i) and distribution of cell cycle were determined using flow cytometry. Results Compared with group C, the cell viability and MMP were significantly decreased, [Ca2+ ]i was significantly increased, the proportion of the cells in G0/G1 phase was significantly decreased, and the proportion of the cells in S and G2/M phases was significantly increased in OGD/R and PP groups (P<0.05). Compared with group OGD/R, the cell viability and MMP were significantly increased, [Ca2+ ]i was significantly decreased, the proportion of the cells in G0/G1 phase was significantly increased, and the proportion of the cells in S and G2/M phases was significantly decreased in group PP (P<0.05). Conclusion The mechanism by which propofol post-conditioning reduces OGD/R-induced apoptosis in hippocampal neurons of rats is associated with inhibition of abnormal cell cycle activation. Key words: Propofol; Cell cycle; Ischemic postconditioning; Neurons; Hippocampus