Propofol inhibits H_2O_2-induced endothelial hyperpermeability

Objective To investigate the protective effect of propofol against H2O2-induced endothelial hyperpermeability.Methods Influence of H2O2 on endothelial permeability were detected by transendothelial electrical resistance(TER)measurement on human umbilical vein endothelial cell(HUVECs)respectively treated with 0,0.2,0.4,0.6and 0.8mmol/L H2O2.HUVECs were randomly divided into control(no treatment),PBS(same volume of PBS),propofol 1(20μmol/L),propofol 2(50μmol/L),propofol 3(100μmol/L)and intralipid(same volume of PBS)group.After30min-pretreatment as described,HUVECs were exposed to 0.6mmol/L H2O2 for 60min.The endothelial permeability,morphologic change of F-actin,phosphorylation of p38 and ERK1/ERK2 were respectively tested by TER,immunofluorescence staining and western blot.Results Marked decreased TER were detected in 0.4 mmol/L,0.6 mmol/L,0.8 mmol/L group H2O2 group(P0.05),and more in 0.6mmol/L,0.8mmol/L group than 0.4mmol/L group(P0.05);H2O2induced the TER obviously decreased from(1.01±0.02)in control group to(0.65±0.05)in group PBS(P0.05).TER in 50μmol/L,100μM propofol treatment group respectively was(0.87±0.04)and(0.90±0.04),which marked risen compared with group PBS(P0.05).H2O2 induced endothelial stress fiber formation and increased p38 and ERK1/ERK2phosphorylation(P0.05),which can be improved by propofol treatment(P0.05).Conclusion Propofol inhibits H2O2-induced endothelial hyperpermeability via p38 and ERK1/ERK2 phosphorylation depression.