Protective Effects of Baicalin on Arsenic Trioxide-induced Oxidative Damage and Apoptosis in Human Umbilical Vein Endothelial Cells
Chung‐Lin Tsai, Chia-Wen Tsai, Wen-Shin Chang, Jiunn‐Cherng Lin, Te‐Chun Hsia, DA-TIAN BAU
Abstract
Background/Aim: Arsenic trioxide (As<sub>2</sub>O<sub>3</sub>) is an environmental pollutant. However, the detailed mechanisms about As<sub>2</sub>O<sub>3</sub>-induced loss of endothelial integrity are unknown. This study aimed at investigating how As<sub>2</sub>O<sub>3</sub> causes endothelial dysfunction and whether baicalin can reverse such dysfunction. Materials and Methods: Human umbilical vein endothelial cells (HUVECs) were used to examine As<sub>2</sub>O<sub>3</sub>-induced oxidative stress, and apoptosis. The influence of baicalin on As<sub>2</sub>O<sub>3</sub>-induced endothelial dysfunction were investigated. Results: The viability of HUVECs was inhibited by As<sub>2</sub>O<sub>3</sub> and cells underwent apoptosis. As<sub>2</sub>O<sub>3</sub> 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 As<sub>2</sub>O<sub>3</sub>-induced apoptosis and As<sub>2</sub>O<sub>3</sub>-suppressed cell viability. Baicalin caused a decrease in NADPH oxidase activity, and re-balanced the ROS level. As<sub>2</sub>O<sub>3</sub>-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 As<sub>2</sub>O<sub>3</sub>-induced cytotoxicity.