Protective Effects of Baicalin on Arsenic Trioxide-induced Oxidative Damage and Apoptosis in Human Umbilical Vein Endothelial Cells.

Abstract

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. 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. The viability of HUVECs was inhibited by As2O3 and cells underwent apoptosis. As2O3 treatment increased NADPH oxidase activity, and elevated the level of reactive oxygen species (ROS). Formamidopyrimidine DNA-glycosylase- 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. Baicalin was found to have the potential capacity to protect endothelial cells from As2O3-induced cytotoxicity.