Résumé
Objective To investigate the mechanism affecting on permeability of vascular endothelial cell by nitric oxide (NO). Methods Series concentration of sin-1（a donor of NO） were added to ECV 304, a cell line of human umbilical vein endothelium. Cell growth and expression of f-actin, a cytoskeleton protein were observed. Results Cell growth was inhibited with a dose from 6.25 to 100 μmol/L and was caused to death at the concentration of 50 to 100 μmol/L by sin-1. The expression of f-actin was suppressed obviously after cultured with 100 μmol/L sin-1 for 4 hours. Conclusion It suggests that anomaly increased NO can increase permeability of blood vessels by suppressing the expression of f-actin, inhibiting cell growth or even resulting in cell death.
Résumé
Objective To investigate the mechanism affecting on permeability of vascular endothelial cell by nitric oxide (NO). Methods Series concentration of sin-1（a donor of NO） were added to ECV 304, a cell line of human umbilical vein endothelium. Cell growth and expression of f-actin, a cytoskeleton protein were observed. Results Cell growth was inhibited with a dose from 6.25 to 100 μmol/L and was caused to death at the concentration of 50 to 100 μmol/L by sin-1. The expression of f-actin was suppressed obviously after cultured with 100 μmol/L sin-1 for 4 hours. Conclusion It suggests that anomaly increased NO can increase permeability of blood vessels by suppressing the expression of f-actin, inhibiting cell growth or even resulting in cell death.