Antioxidant XXXX dismutase attenuates increased endothelial permeability induced by platelet-activating factor.

@entity1 @entity3545 @entity11177 @entity2625 @entity5567 @entity224
To study the protective effects of the antioxidant @entity224 dismutase (SOD) against platelet-activating factor ( @entity5567 )-induced endothelial permeability. Endothelial cells (ECs) were isolated from @entity1 umbilical veins from normal pregnancies. The first passage (P1) ECs were grown in polycarbonate transwell filters. Confluent ECs were incubated with @entity5567 at concentrations of 2, 5, and 10 microgram/mL for 2 hours or pretreated with @entity224 dismutase. Endothelial monolayer permeability was then measured by EC electrical resistance or by the leakage of horseradish @entity2625 (HRP) passing through filters. Endothelial junctional protein distribution and expression of @entity3545 and @entity11177 were determined by fluorescent staining of endothelial monolayer and by Western blot analysis. mRNA expressions for @entity3545 and @entity11177 were determined by reverse transcriptase-polymerase chain reaction. Data are expressed as Omega. cm(2) for electrical resistance and DeltaOD 470 nm for HRP assay and presented as mean +/- standard error of the mean. Analysis of variance was used for statistical analysis. A P value less than.05 was considered statistically significant. Endothelial cell electrical resistance was decreased and HRP leakage was increased in ECs treated with @entity5567 . Intercellular gaps were formed at cell contact regions in ECs treated with @entity5567 , as evaluated by staining of junctional protein @entity3545 and @entity11177 . The functional changes of the EC barrier and the formation of intercellular gaps induced by @entity5567 were concentration dependent, which could be partially attenuated by pretreatment of ECs with SOD. Total cellular junctional protein expression and mRNA expression of @entity3545 and @entity11177 were not affected by @entity5567 . Increased EC monolayer permeability induced by platelet-activating factor is associated with disorganization of EC junctional protein distribution of @entity3545 and @entity11177 . @entity224 dismutase partially attenuated the @entity5567 -induced increased endothelial monolayer permeability, which suggests that oxidative stress might be involved in the process of @entity5567 -induced disturbances of endothelial barrier function.
