Effect of propofol on mitochondrial fission in a rat hippocampal neuron model of hypoxia/reoxygenation injury

Objective To evaluate the effect of propofol on mitochondrial fission in a rat hippocampal neuron model of hypoxia/reoxygenation (H/R) injury. Methods Primarily cultured hippocampal neurons of neonatal Sprague-Dawley rats were randomly divided into 4 groups (n= 42 each) using a random number table: control group (group C); vehicle group (group V); H/R group; H/R+ propofol group (group H/R+ P). In group V, H/R was not produced, the vehicle dimethyl sulfoxide with the final concentration of 0.01% was added, and the cells were then incubated for 6 h. In group H/R, the hippocampal neurons were subjected to oxygen-glucose deprivation for 6 h followed by 20 h reoxygenation.In group H/R+ P, propofol with the final concentration of 1 μmol/L was added at 6 h of hypoxia.At 20 h of reoxygenation, the cell apoptosis (using flow cytometry), Ca2+ concentrations in cytoplasm (with the laser scanning confocal microscope), calcineurin (CaN) activities (by enzyme-linked immunosorbent assay), and expression of mitochondrial fission proteins dynamin-related protein 1 (Drp1) and fission 1 (Fis1), and apoptosis-related proteins cytochrome c (Cyt c) and apoptosis-inducing factor (AIF) (by Western blot) were measured.The apoptotic rate was calculated. Results Compared with group C, the apoptotic rate, Ca2+ concentrations, CaN activities, and expression of Drp1, Fis1, Cyt c and AIF were significantly increased in H/R and H/R+ P groups (P 0.05). Compared with group H/R, the apoptotic rate, Ca2+ concentrations, CaN activities, and expression of Drp1, Fis1, Cyt c and AIF were significantly decreased in group H/R+ P (P<0.05=. Conclusion Propofol can reduce the H/R injury to rat hippocampal neurons through inhibiting mitochondrial fission. Key words: Propofol; Anoxia; Mitochondria; Hippocampus; Neurons