Influence of propofol on endotoxin-induced expression of VEGF receptor 2 in renal glomerular endothelial cells of rats

Objective To investigate the influence of propofol on endotoxin-induced expression of vascular endothelial growth factor (VEGF)receptor 2 in renal glomerular endothelial cells of rats. Methods The primarily cultured renal glomerular endothelial cells of Sprague-Dawley rats were seeded in 24-well plates at a density of 1×106 cells/ml (200 μl/well) and divided into 6 groups (n = 35 each) using a random number table: control group (group C); introlipid group (group I); propofol group (group P); lipopolysaccharide (LPS) group (group L); LPS + introlipid group (group L+ I); LPS + propofol group (group L+ P). In group I, 10% introlipid was added with the final concentration of 4 μg/ml. In group P, propofol was added with the final concentration of 4 μg/ml. In group L, LPS was added with the final concentration of 10 μg/ml. In group L+ I, 10% introlipid was added with the final concentration of 4 μg/ml at 30 min before LPS with the final concentration of 10 μg/ml was added. In group L+ P, propofol was added with the final concentration of 4 μg/ml at 30 min before LPS with the final concentration of 10 μg/ml was added. After 6 h of incutation, the cells were collected for measurement of cell permeability and VEGF receptor 2 mRNA expression (using RT-PCR), VEGF receptor 2 protein expression (by Western blot), and for examination of the morphology of cytoskeletal protein filamentous-actin (F-actin) with confocal microscope (by immunofluorescence). Results Compared with group C, the expression of VEGF receptor 2 mRNA and protein was significantly up-regulated, and the cell permeability was increased in L, L+ I and L+ P groups, and no significant changes were found in the parameters mentioned above in I and P groups. Compared with group L, the expression of VEGF receptor 2 mRNA and protein was significantly down-regulated, and the cell permeability was decreased in L+ P group, and no significant changes were found in L+ I group. F-actin connected closely between adjacent cells and a dense peripheral F-actin band was formed in C, I and P groups, while F-actin depolymerized, the peripheral F-actin band was disrupted, and cells shrank in L and L+ I groups. In group L+ P, a tighter intercellular connection of F-actin was observed and cytoskeleton was found to be intact. Conclusion Propofol can inhibit endotoxin-induced increase in the permeability of renal glomerular endothelial cells through down-regulating the expression of VEGF receptor 2 in rats. Key words: Propofol; Vascular endothelial growth factor receptor-2; Endotoxemia; Endothelial cells; Kidney glomerulus