Abstract: AIM: To investigate the effects of propofol on the expression of protien kinase C and intracellular calcium homeostasis in human vascular endothelial cells induced by hypoxia-reoxygenation injury. METHODS: The endothelial cells were separated from human umbilical veins.The cells were cultured in normal medium or the medium containing different concentrations of propofol. The cells were further incubated in hypoxic condition for 30 min and then in normal condition for 6 h to induce hypoxia-reoxygenation injury.The cells were divided into groups:the control group (C group), the hypoxia-reoxygenation group (HR group) and propofol groups (PR 25, 50, 100 μmol L groups).The expression of PKC and the concentration of intracellular calcium were measured by Western-blot analysis and immunofluorescence method, respectively. RESULTS: The number of apoptosis increased after reoxygenation (14.7±1.0 %).Propofol inhibited the apoptosis significantly (P<0.01), and the inhibited effect of propofol on 50 μmol L(9.4±0.6) % and 100 μmol L(9.5±0.6) %was more significant compared with the propofol on 25 μmol L(12.3±0.7) % (P<0.01).The expression of PKC was significantly inhibited after reoxygenation (P<0.01).The concentration of intracellular calcium induced by hypoxia-reoxygenation injury was up-regulated (117.3±6.0) %.Propofol attenuated the concentration of intracellular calcium significantly (P<0.01) and was more effective at 50 and 100 μmol L (P<0.01).Propofol at a concentration of 25 μmol L could significantly (19.0±1.7) %upregulate the expression of PKC (P<0.01).Propofol at concentrations of 50 μmol L (27.0±2.4) % and 100 μmol L (27.5± 2.6) % showed a similar result but is significant compared with PR25 group (P<0.01). CONCLUSION: Hypoxia-reoxygenation injury induces apoptosis, which may be related to inhibiting the expression of PKC and increasing the concentration of intracellular calcium.Propofol inhibits the apoptosis of endothelial cells induced by hypoxia-reoxygenation injury, and the mechanism is possibly related to the activation of PKC and depression of calcium overload.

Key words: propofol, endothelial cells, anoxia, apoptosis