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 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.

Conclusion: Baicalin was found to have the potential capacity to protect endothelial cells from As₂O₃-induced cytotoxicity.

Keywords: Apoptosis; arsenic trioxide; baicalin; human umbilical vein endothelial cells; oxidative damage.