Effect of propofol post-conditioning on oxygen-glucose deprivation and restoration-induced abnormal cell cycle activation in hippocampal neurons of rats / 中华麻醉学杂志

ABSTRACT

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 5×105cells∕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 1.2μg∕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 signifi? cantly 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). Com?pared with group OGD∕R, the cell viability and MMP were significantly increased, [ Ca2+] i was significant?ly 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.