Protective effects of baicalin on arsenic trioxide-induced oxidative damage and apoptosis in human umbilical vein endothelial cells

Abstract

Background/Aim: Arsenic trioxide (As2O3) is an environmental pollutant. However, the detailed mechanisms about As2O3-induced loss of endothelial integrity are unknown. This study aimed at investigating how As2O3. causes endothelial dysfunction and whether baicalin can reverse such dysfunction. Materials and Methods: Human umbilical vein endothelial cells (HUVECs) were used to examine As2O3- induced oxidative stress, and apoptosis. The influence of baicalin on As2O3-induced endothelial dysfunction were investigated. Results: The viability of HUVECs was inhibited by As2O3and cells underwent apoptosis. As2O3treatment increased NADPH oxidase activity, and elevated the level of reactive oxygen species (ROS). Formamidopyrimidine DNAglycosylase- and endonuclease III-digestible adducts were accumulated. Baicalin reversed As2O3-induced apoptosis and As2O3-suppressed cell viability. Baicalin caused a decrease in NADPH oxidase activity, and re-balanced the ROS level. As2O3-induced formamidopyrimidine DNA-glycosylase- and endonuclease III-digestible adducts were down-regulated. Conclusion: Baicalin was found to have the potential capacity to protect endothelial cells from As2O3-induced cytotoxicity.