Protective effect of propofol against H 2O 2 potentiated TNF-alpha induced human vascular endothelial cell apoptosis

Abstract

Objective: To test the hypothesis that oxygen free radicals can potentiate TNF-α cellular toxicity, which might be reserved by propofol in human vascular endothelial cells. Methods: Cultured human ECV304 cells were divided into five groups: untreated (Control), treated with 10 μmol/L hydrogen peroxide (H 2O 2) and treated with 40 nmol/L TNF-α alone (T) or in the presence of H 2O 2 (T+H) or in propofol + H 2O 2 (T+H+P), with each cultured for 24 hours. Cell apoptosis was assessed by flow cytometry. The concentration of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were detected at the same time. Results: H 2O 2, at 10 μmol/L, did not cause significant lipid peroxidation, but enhanced TNF-α induced cell apoptosis (P<0.01). Propofol at 50 μmol/L attenuated TNF-α and H 2O 2 induced cell apoptosis, accompanied with a decrease in MDA, while with increases in SOD and GSH-Px. Conclusion: H 2O 2, even at trace concentration, may significantly enhance TNF-α induced endothelial cell apoptosis. Propofol exerts protective effects against H 2O 2 potentiated TNF-α cell toxicity by reduction of oxidative injury.