Protective Effects of Captopril Against Hydrogen Peroxide-induced Disruption of Tight Junctions in ECV304 Monolayers

Abstract

Angiotensin-converting enzyme (ACE) inhibitors demonstrated various beneficial
actions on vascular structure and function beyond their blood pressure-lowering effects. In
this study, we investigated the protective effect of captopril on hydrogen peroxide (H2O2)-
induced dysfunction of endothelial barriers, using an in vitro model of ECV304 cells.
Treatment the ECV304 monolayers with H2O2 for 4 hr at the noncytotoxic concentration of
200 micromolar, resulting in the loss of TEER values and tight junction proteins occludin and
zonular occluden (ZO)-1. Pretreatment the cells with captopril for 30 min prior to H2O2
attenuated the loss of TEER values in concentration dependent manner. The
immunofluorescent visualization revealed that captopril prevented the H2O2-mediated loss of
expression and localization of occludin and ZO-1 at the cell borders. Our results suggested
that captopril could protect the barrier function of ECV304 monolayers from oxidative stress
through preventing the loss of tight junction proteins. Consequently, the integrity of tight
junction structure was preserved during oxidative assault.