PT - JOURNAL ARTICLE AU - CHUNG-LIN TSAI AU - CHIA-WEN TSAI AU - WEN-SHIN CHANG AU - JIUNN-CHERNG LIN AU - TE-CHUN HSIA AU - DA-TIAN BAU TI - Protective Effects of Baicalin on Arsenic Trioxide-induced Oxidative Damage and Apoptosis in Human Umbilical Vein Endothelial Cells AID - 10.21873/invivo.12243 DP - 2021 Jan 01 TA - In Vivo PG - 155--162 VI - 35 IP - 1 4099 - http://iv.iiarjournals.org/content/35/1/155.short 4100 - http://iv.iiarjournals.org/content/35/1/155.full SO - In Vivo2021 Jan 01; 35 AB - 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.