DA-Tian Bau1,2,3, Chung-Lin Tsai4,5, Chia-Wen Tsai2, Wen-Shin Chang2, Jiunn-Cherng Lin6, Te-Chun Hsia2. 1. Graduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan, R.O.C.; datian@mail.cmuh.org.tw artbau2@gmail.com. 2. Terry Fox Cancer Research Laboratory, Department of Medical Research, China Medical University Hospital, Taichung, Taiwan, R.O.C. 3. Department of Bioinformatics and Medical Engineering, Asia University, Taichung, Taiwan, R.O.C. 4. Graduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan, R.O.C. 5. Division of Cardiac and Vascular Surgery, Cardiovascular Center, Taichung Veterans General Hospital, Taichung, Taiwan, R.O.C. 6. Division of Cardiology, Department of Internal Medicine, Taichung Veterans General Hospital Chiayi Branch, Chiayi, Taiwan, R.O.C.
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. Copyright
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:Humanumbilical 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. Copyright
Authors: Shu Liu; Hua Shen; Ming Xu; Ou Liu; Limin Zhao; Sa Liu; Zhenheng Guo; Jie Du Journal: Am J Physiol Endocrinol Metab Date: 2010-06-08 Impact factor: 4.310