This study was performed to examine 1) whether propofol prevented the increases in intracellular calcium and radical oxygen species (ROS) induced by lysophosphatidic acid (LPA) in endothelial cell; 2) whether these two types of increases were mediated by common underlying mechanisms.

Intracellular Ca²⁺ ([Ca²⁺]_i) and H₂O₂ were measured in endothelial cell line (ECV 304) using a laser scanning confocal microscope. The cells, cultured and serum-starved on round coverslips, were incubated with various concentrations of propofol for 30 minutes, and then stimulated with various concentrations of LPA. The samples were excited by a 488 nm argon laser and images were filtered by a 515 nm longpass emission filter. The results were expressed as relative fluorescence intensity (RFI) and fold stimulation (fold).

LPA increased in intracellular ROS in the endothelial cell in a dose-dependent manner. In addition, LPA-induced increase in ROS were alleviated by ROS scavengers such as Aspergillus niger catalase and n-(2-mercaptopropionyl)-glycine (2-MPG). LPA also increased in [Ca²⁺]_i in a dose-dependent fashion. Propofol prevented LPA-induced increase in ROS and [Ca²⁺]_i whereas 2-MPG did not affect the change of calcium level induced by LPA application.

These results suggested that propofol prevented the increases in intracellular calcium and ROS induced by LPA in endothelial cell, and these two types of increases might be mediated by different underlying mechanisms.