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Korean Journal of Anesthesiology 2004;46(6):S4-S9.
DOI: https://doi.org/10.4097/kjae.2004.46.6.S4   
Preventive Effects of Propofol Aganinst the Elevation of Intracellular Ca2+ and Reactive Oxygen Species Induced by Lysophosphatidic Acid in Endothelial Cells.
Tae Gan Ryu, Nan Suk Kim, Young Don Min, Kwon Soo Ha, Myoung Hoon Kong, Sang Ho Lim
1Department of Anesthesiology and Pain Medicine, Korea University School of Medicine, Seoul, Korea.
2Department of Molecular and Cellular Biochemistry, Kangwon National University School of Medicine, Chuncheon, Gangwon-do, Korea.
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.
Key Words: propofol; endothelial cell; calcium; reactive oxygen species; lysophosphatidic acid


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